Cardiovascular effects of dobutamine,norepinephrine and phenylephrine in isoflurane-anaesthetized dogs administered dexmedetomidine–vatinoxan

ObjectiveTo determine whether dobutamine, norepinephrine or phenylephrine infusions alleviate hypotension in isoflurane-anaesthetized dogs administered dexmedetomidine with vatinoxan.Study designBalanced, randomized crossover trial.AnimalsA total of eight healthy Beagle dogs.MethodsEach dog was anaesthetized with isoflurane (end-tidal isoflurane 1.3%) and five treatments: dexmedetomidine hydrochloride (2.5 μg kg^–1) bolus followed by 0.9% saline infusion (DEX-S); dexmedetomidine and vatinoxan hydrochloride (100 μg kg^–1) bolus followed by an infusion of 0.9% saline (DEX-VAT-S), dobutamine (DEX-VAT-D), norepinephrine (DEX-VAT-N) or phenylephrine (DEX-VAT-P). The dexmedetomidine and vatinoxan boluses were administered at baseline (T0) and the treatment infusion was started after 15 minutes (T15) if mean arterial pressure (MAP) was < 90 mmHg. The treatment infusion rate was adjusted every 5 minutes as required. Systemic haemodynamics were recorded at T0 and 10 (T10) and 45 (T45) minutes. A repeated measures analysis of covariance model was used.ResultsMost dogs had a MAP < 70 mmHg at T0 before treatment. Treatments DEX-S and DEX-VAT all significantly increased MAP at T10, but systemic vascular resistance index (SVRI) was significantly higher and cardiac index (CI) lower after DEX-S than after DEX-VAT. CI did not significantly differ between DEX-S and DEX-VAT-S at T45, while SVRI remained higher with DEX-S. Normotension was achieved by all vasoactive infusions in every dog, whereas MAP was below baseline with DEX-VAT-S, and higher than baseline with DEX-S at T45. Median infusion rates were 3.75, 0.25 and 0.5 μg kg^–1 minute^–1 for dobutamine, norepinephrine and phenylephrine, respectively. Dobutamine and norepinephrine increased CI (mean ± standard deviation, 3.35 ± 0.70 and 3.97 ± 1.24 L minute^–1 m^–2, respectively) and decreased SVRI, whereas phenylephrine had the opposite effect (CI 2.13 ± 0.45 L minute^–1 m^–2).Conclusions and clinical relevanceHypotension in isoflurane-anaesthetized dogs administered dexmedetomidine and vatinoxan can be treated with either dobutamine or norepinephrine.     

Anti‐nociceptive and sedative effects of romifidine,tramadol and their combination administered intravenously slowly in ponies

ObjectiveTo evaluate the anti-nociceptive and sedative effects of slow intravenous (IV) injection of tramadol, romifidine, or a combination of both drugs in ponies.Study designWithin-subject blinded.AnimalsTwenty ponies (seven male, 13 female, weighing mean ± SD 268.0 ± 128 kg).MethodsOn separate occasions, each pony received one of the following three treatments IV; romifidine 50 μg kg⁻ (R) tramadol 3 mg kg⁻¹ given over 15 minutes (T) or tramadol 3 mg kg⁻¹followed by romifidine 50 μg kg⁻¹ (RT). Physiologic parameters and caecal borborygmi (CB) were measured and sedation and response to electrical stimulation of the coronary band assessed before and up to 120 minutes following drugs administration. Results were analyzed using the Friedman’s test and 2 way anova as relevant.ResultsWhen compared to baseline, heart (HR, beats minute⁻¹) and respiratory rates (f_R, breaths minute⁻¹) increased with treatment T (highest mean ± SD, HR 43 ± 1; f_R 33 ± 2) and decreased with R (lowest HR 29 ± 1 and f_R 10 ± 4) and RT (lowest HR 32 ± 1 and f_R 9 ± 3). There were no changes in other measured physiological variables. The height of head from the ground was lower following treatments R and TR than T. There was slight ataxia with all three treatments. No excitatory behavioural effects were observed. The response to electrical stimulation was reduced for a prolonged period relative to baseline following all three treatments, the effect being significantly greatest with treatment RT.ConclusionTramadol combined with romifidine at the stated doses proved an effective sedative and anti-nociceptive combination in ponies, with no unacceptable behavioural or physiologic side effects.Clinical relevanceSlow controlled administration of tramadol should reduce the occurrence of adverse behavioural side effects.     

Evaluation of medetomidine-ketamine and dexmedetomidine-ketamine in Chinese water deer (Hydropotes inermis)

ObjectiveTo investigate physiological and sedative/immobilization effects of medetomidine or dexmedetomidine combined with ketamine in free-ranging Chinese water deer (CWD).Study designProspective clinical trial.Animals10 free-ranging adult Chinese water deer (11.0 ± 2.6 kg).MethodsAnimals were darted intramuscularly with 0.08 ± 0.004 mg kg^?1 medetomidine and 3.2 ± 0.2 mg kg^?1 ketamine (MK) or 0.04 ± 0.01 mg kg^?1 dexmedetomidine and 2.9 ± 0.1 mg kg^?1 ketamine (DMK) If the animal was still laterally recumbent after 60 minutes of immobilization, atipamezole was administered intravenously (MK: 0.4 ± 0.02 mg kg^?1, DMK: 0.2 ± 0.03 mg kg^?1). Heart rate (HR) respiratory rate (f_R) and temperature were recorded at 5-minute intervals. Arterial blood was taken 15 and 45 minutes after initial injection. Statistical analysis was performed using Student’s t-test or anova. p < 0.05 was considered significant.ResultsAnimals became recumbent rapidly in both groups. Most had involuntary ear twitches, but there was no response to external stimuli. There were no statistical differences in mean HR (MK: 75 ± 14 beats minute^?1; DMK: 85 ± 21 beats minute^?1), f_R (MK: 51 ± 35 breaths minute^?1; DMK; 36 ± 9 breaths minute^?1), temperature (MK: 38.1 ± 0.7 °C; DMK: 38.4 ± 0.5 °C), blood gas values (MK: PaO₂ 63 ± 6 mmHg, PaCO₂ 49.6 ± 2.6 mmHg, HCO₃^? 30.8 ± 4.5 mmol L^?1; DMK: PaO₂ 77 ± 35 mmHg, PaCO₂ 45.9 ± 11.5 mmHg, HCO₃^? 31.0 ± 4.5 mmol L^?1) and biochemical values between groups but temperature decreased in both groups. All animals needed antagonism of immobilization after 60 minutes. Recovery was quick and uneventful. There were no adverse effects after recovery.Conclusion and clinical relevanceBoth anaesthetic protocols provided satisfactory immobilisation. There was no clear preference for either protocol and both appear suitable for CWD.     

Cardiovascular,respiratory, electrolyte and acid–base balance during continuous dexmedetomidine infusion in anesthetized dogs

ObjectiveTo evaluate the cardiovascular, respiratory, electrolyte and acid–base effects of a continuous infusion of dexmedetomidine during propofol–isoflurane anesthesia following premedication with dexmedetomidine.Study designProspective experimental study.AnimalsFive adult male Walker Hound dogs 1–2 years of age averaging 25.4 ± 3.6 kg.MethodsDogs were sedated with dexmedetomidine 10 μg kg^?1 IM, 78 ± 2.3 minutes (mean ± SD) before general anesthesia. Anesthesia was induced with propofol (2.5 ± 0.5 mg kg^?1) IV and maintained with 1.5% isoflurane. Thirty minutes later dexmedetomidine 0.5 μg kg^?1 IV was administered over 5 minutes followed by an infusion of 0.5 μg kg^?1 hour^?1. Cardiac output (CO), heart rate (HR), ECG, direct blood pressure, body temperature, respiratory parameters, acid–base and arterial blood gases and electrolytes were measured 30 and 60 minutes after the infusion started. Data were analyzed via multiple linear regression modeling of individual variables over time, compared to anesthetized baseline values. Data are presented as mean ± SD.ResultsNo statistical difference from baseline for any parameter was measured at any time point. Baseline CO, HR and mean arterial blood pressure (MAP) before infusion were 3.11 ± 0.9 L minute^?1, 78 ± 18 beats minute^?1 and 96 ± 10 mmHg, respectively. During infusion CO, HR and MAP were 3.20 ± 0.83 L minute^?1, 78 ± 14 beats minute^?1 and 89 ± 16 mmHg, respectively. No differences were found in respiratory rates, PaO₂, PaCO₂, pH, base excess, bicarbonate, sodium, potassium, chloride, calcium or lactate measurements before or during infusion.Conclusions and clinical relevanceDexmedetomidine infusion using a loading dose of 0.5 μg kg^?1 IV followed by a constant rate infusion of 0.5 μg kg^?1 hour^?1 does not cause any significant changes beyond those associated with an IM premedication dose of 10 μg kg^?1, in propofol–isoflurane anesthetized dogs. IM dexmedetomidine given 108 ± 2 minutes before onset of infusion showed typical significant effects on cardiovascular parameters.     

Propofol and fentanyl infusions in dogs of various breeds undergoing surgery

ObjectiveTo report the cardiovascular variables, anaesthetic effects and recovery quality of an anaesthesia technique using variable rate infusion propofol combined with constant rate infusion fentanyl in dogs undergoing elective surgery.Study designProspective clinical trial.AnimalsA total of 27 dogs, aged 2.7 ± 2.65 years and weighing 24 ± 11 kg.MethodsFollowing intramuscular acepromazine (0.03 or 0.05 mg kg^?1) and subcutaneous carprofen (4 mg kg^?1) pre-medication, anaesthesia was induced with propofol (4.0 ± 0.5 mg kg^?1) intravenously (IV). All dogs were ventilated with 100% oxygen to maintain normocapnia. Propofol was infused at 0.4 mg kg^?1 minute^?1 for 20 minutes and then at 0.3 mg kg^?1minute^?1. If mean arterial blood pressure (MAP) decreased below 70 mmHg, propofol infusion was reduced by 0.1 mg kg^?1 minute^?1. Five minutes after induction of anaesthesia, fentanyl was administered (2 μg kg^?1) IV followed by the infusion at 0.5 μg kg^?1 minute^?1 and atropine (40 μg kg^?1) IV. Heart rate, MAP, respiratory rate, tidal volume, end-tidal carbon dioxide, presence of reflexes, movements and recovery times and quality were recorded.ResultsMean anaesthetic duration was 131 ± 38.5 minutes. Mean heart rate peaked 10 minutes after atropine injection and gradually declined, reaching pre-anaesthetic values at 55 minutes. MAP easily was maintained above 70 mmHg. Mean times to return of spontaneous ventilation, extubation, head lift and sternal recumbency were 21 ± 10.1, 33 ± 14.6, 43 ± 19.7 and 65 ± 23.4 minutes, respectively. Recovery was smooth and quiet. The time to sternal recumbency was significantly correlated with the duration of anaesthesia and total dose of propofol; time to extubation was correlated to total dose of propofol.Conclusion and clinical relevancePropofol and fentanyl infusions provided stable cardiovascular function and satisfactory conditions for surgery. Some modifications of infusion rates are required to improve the long-recovery times.     

Electrocardiographic and cardiopulmonary effects of intramuscular administration of glycopyrrolate and romifidine in conscious beagle dogs

Objective To determine the electrocardiographic and cardiopulmonary effects of IM administration of romifidine with and without prior administration of glycopyrrolate in conscious dogs. Study design Prospective randomized study. Animals Twelve healthy, adult beagles. Materials and methods Dogs were assigned at random to each of three treatments with glycopyrrolate (six dogs), and to each of three treatments without glycopyrrolate (six dogs). Baseline data were recorded, and saline solution or glycopyrrolate (10 µg kg^–1) was given IM. After 15 minutes, saline solution (control) or romifidine (20 or 40 µg kg^–1) was given IM. An ECG, heart rate (HR), systemic blood pressures, and respiratory rate (RR) were recorded before and 2.5, 5, 10, 15, 30, 45, 60, 75, 90, 105 and 120 minutes after romifidine administration. Rectal temperature (RT), pH, PaCO₂, PaO₂, hematocrit and plasma protein were determined before and 15, 30, 60 and 120 minutes after romifidine administration. Data were analyzed using analysis of variance for repeated measures and Tukey multiple comparison tests. Results Without glycopyrrolate, HR (beats minute^–1) decreased to minimum values (mean ± SD) of 52 ± 7 and 49 ± 12 (control 89 ± 20) 45 minutes after administration of romifidine at doses of 20 and 40 µg kg^–1, respectively. Sinus bradycardia (HR < 60 beats minute^–1), which persisted for up to 120 minutes, was observed in five of six and six of six dogs given romifidine at doses of 20 and 40 µg kg^–1, respectively. With glycopyrrolate, decreases in HR were prevented and mean arterial pressure (mm Hg) increased to maximum values of 139 ± 25 and 173 ± 17 (control 113 ± 11) 30 minutes after administration of romifidine at doses of 20 and 40 µg kg^–1, respectively. With and without glycopyrrolate, RR did not change appreciably, RT decreased, and pH, PaCO₂, PaO₂, hematocrit and plasma protein did not change after administration of romifidine. Conclusions and clinical relevance In healthy conscious beagles, IM administration of romifidine at doses of 20 and 40 µg kg^–1 causes sinus bradycardia which persists for up to 120 minutes. Administration of glycopyrrolate 15 minutes before administration of romifidine, prevents sinus bradycardia and induces moderate increases in arterial pressure.     

Cardiovascular effects of epidural administration of methadone, ropivacaine 0.75% and their combination in isoflurane anaesthetized dogs

ObjectiveTo compare the cardiovascular effects of four epidural treatments in isoflurane anaesthetised dogs.Study designProspective, randomized. experimental study.AnimalsSix female, neutered Beagle dogs (13.3 ± 1.0 kg), aged 3.6 ± 0.1 years.MethodsAnaesthesia was induced with propofol (8.3 ± 1.1 mg kg^?1) and maintained with isoflurane in a mixture of oxygen and air [inspiratory fraction of oxygen (FiO₂) = 40%], using intermittent positive pressure ventilation. Using a cross-over model, NaCl 0.9% (P); methadone 1% 0.1 mg kg^?1 (M); ropivacaine 0.75% 1.65 mg kg^?1 (R) or methadone 1% 0.1 mg kg^?1 + ropivacaine 0.75% 1.65 mg kg^?1 (RM) in equal volumes (0.23 mL kg^?1) using NaCl 0.9%, was administered epidurally at the level of the lumbosacral space. Treatment P was administered to five dogs only. Cardiovascular and respiratory variables, blood gases, and oesophageal temperature were recorded at T-15 and for 60 minutes after epidural injection (T0).ResultsMean overall heart rate (HR in beats minute^?1) was significantly lower after treatment M (119 ± 16) (p = 0.0019), R (110 ± 18) (p < 0.0001) and RM (109 ± 13) (p < 0.0001), compared to treatment P (135 ± 21). Additionally, a significant difference in HR between treatments RM and M was found (p = 0.04). After both ropivacaine treatments, systemic arterial pressures (sAP) were significantly lower compared to other treatments. No significant overall differences between treatments were present for central venous pressure, cardiac output, stroke volume, systemic vascular resistance, oxygen delivery and arterial oxygen content (CaO₂). Heart rate and sAP significantly increased after treatment P and M compared to baseline (T-15). With all treatments significant reductions from baseline were observed in oesophageal temperature, packed cell volume and CaO₂. A transient unilateral Horner’s syndrome occurred in one dog after treatment R.Conclusions and clinical relevanceClinically important low sAPs were observed after the ropivacaine epidural treatments in isoflurane anaesthetised dogs. Systemic arterial pressures were clinically acceptable when using epidural methadone.     

Cardiopulmonary and isoflurane‐sparing effects of epidural or intravenous infusion of dexmedetomidine in cats undergoing surgery with epidural lidocaine

ObjectiveTo compare the cardiorespiratory, anesthetic-sparing effects and quality of anesthetic recovery after epidural and constant rate intravenous (IV) infusion of dexmedetomidine (DEX) in cats given a low dose of epidural lidocaine under propofol-isoflurane anesthesia and submitted to elective ovariohysterectomy.Study designRandomized, blinded clinical trial.AnimalsTwenty-one adult female cats (mean body weight: 3.1 ± 0.4 kg).MethodsCats received DEX (4 μg kg^?1, IM). Fifteen minutes later, anesthesia was induced with propofol and maintained with isoflurane. Cats were divided into three groups. In GI cats received epidural lidocaine (1 mg kg^?1, n = 7), in GII cats were given epidural lidocaine (1 mg kg^?1) + DEX (4 μg kg^?1, n = 7), and in GIII cats were given epidural lidocaine (1 mg kg^?1) + IV constant rate infusion (CRI) of DEX (0.25 μg kg^?1 minute^?1, n = 7). Variables evaluated included heart rate (HR), respiratory rate (f_R), systemic arterial pressures, rectal temperature (RT), end-tidal CO₂, end-tidal isoflurane concentration (e′ISO), arterial blood gases, and muscle tone. Anesthetic recovery was compared among groups by evaluation of times to recovery, HR, f_R, RT, and degree of analgesia. A paired t-test was used to evaluate pre-medication variables and blood gases within groups. anova was used to compare parametric data, whereas Friedman test was used to compare muscle relaxation.ResultsEpidural and CRI of DEX reduced HR during anesthesia maintenance. Mean ± SD e′ISO ranged from 0.86 ± 0.28% to 1.91 ± 0.63% in GI, from 0.70 ± 0.12% to 0.97 ± 0.20% in GII, and from 0.69 ± 0.12% to 1.17 ± 0.25% in GIII. Cats in GII and GIII had longer recovery periods than in GI.Conclusions and clinical relevanceEpidural and CRI of DEX significantly decreased isoflurane consumption and resulted in recovery of better quality and longer duration, despite bradycardia, without changes in systemic blood pressure.     

Effects of vatinoxan in dogs premedicated with medetomidine and butorphanol followed by sevoflurane anaesthesia: a randomized clinical study

ObjectiveTo investigate effects of vatinoxan in dogs, when administered as intravenous (IV) premedication with medetomidine and butorphanol before anaesthesia for surgical castration.Study designA randomized, controlled, blinded, clinical trial.AnimalsA total of 28 client-owned dogs.MethodsDogs were premedicated with medetomidine (0.125 mg m^?2) and butorphanol (0.2 mg kg^?1) (group MB; n = 14), or medetomidine (0.25 mg m^?2), butorphanol (0.2 mg kg^?1) and vatinoxan (5 mg m^?2) (group MB-VATI; n = 14). Anaesthesia was induced 15 minutes later with propofol and maintained with sevoflurane in oxygen (targeting 1.3%). Before surgical incision, lidocaine (2 mg kg^?1) was injected intratesticularly. At the end of the procedure, meloxicam (0.2 mg kg^?1) was administered IV. The level of sedation, the qualities of induction, intubation and recovery, and Glasgow Composite Pain Scale short form (GCPS-SF) were assessed. Heart rate (HR), respiratory rate (f_R), mean arterial pressure (MAP), end-tidal concentration of sevoflurane (Fe′Sevo) and carbon dioxide (Pe′CO₂) were recorded. Blood samples were collected at 10 and 30 minutes after premedication for plasma medetomidine and butorphanol concentrations.ResultsAt the beginning of surgery, HR was 61 ± 16 and 93 ± 23 beats minute^?1 (p = 0.001), and MAP was 78 ± 7 and 56 ± 7 mmHg (p = 0.001) in MB and MB-VATI groups, respectively. No differences were detected in f_R, Pe′CO₂, Fe′Sevo, the level of sedation, the qualities of induction, intubation and recovery, or in GCPS-SF. Plasma medetomidine concentrations were higher in group MB-VATI than in MB at 10 minutes (p = 0.002) and 30 minutes (p = 0.0001). Plasma butorphanol concentrations were not different between groups.Conclusions and clinical relevanceIn group MB, HR was significantly lower than in group MB-VATI. Hypotension detected in group MB-VATI during sevoflurane anaesthesia was clinically the most significant difference between groups.     

Assessing the influence of mechanical ventilation on blood gases and blood pressure in rattlesnakes

ObjectiveTo characterize the impact of mechanical positive pressure ventilation on heart rate (HR), arterial blood pressure, blood gases, lactate, glucose, sodium, potassium and calcium concentrations in rattlesnakes during anesthesia and the subsequent recovery period.Study designProspective, randomized trial.AnimalsTwenty one fasted adult South American rattlesnakes (Crotalus durissus terrificus).MethodsSnakes were anesthetized with propofol (15 mg kg⁻¹) intravenously, endotracheally intubated and assigned to one of four ventilation regimens: Spontaneous ventilation, or mechanical ventilation at a tidal volume of 30 mL kg⁻¹ at 1 breath every 90 seconds, 5 breaths minute⁻¹, or 15 breaths minute⁻¹. Arterial blood was collected from indwelling catheters at 30, 40, and 60 minutes and 2, 6, and 24 hours following induction of anesthesia and analyzed for pH, PaO₂, PaCO₂, and selected variables. Mean arterial blood pressure (MAP) and HR were recorded at 30, 40, 60 minutes and 24 hours.ResultsSpontaneous ventilation and 1 breath every 90 seconds resulted in a mild hypercapnia (PaCO₂ 22.4 ± 4.3 mmHg [3.0 ± 0.6 kPa] and 24.5 ± 1.6 mmHg [3.3 ± 0.2 kPa], respectively), 5 breaths minute⁻¹ resulted in normocapnia (14.2 ± 2.7 mmHg [1.9 ± 0.4 kPa]), while 15 breaths minute⁻¹ caused marked hypocapnia (8.2 ± 2.5 mmHg [1.1 ± 0.3 kPa]). Following recovery, blood gases of the four groups were similar from 2 hours. Anesthesia, independent of ventilation was associated with significantly elevated glucose, lactate and potassium concentrations compared to values at 24 hours (p < 0.0001). MAP increased significantly with increasing ventilation frequency (p < 0.001). HR did not vary among regimens.Conclusions and clinical relevanceMechanical ventilation had a profound impact on blood gases and blood pressure. The results support the use of mechanical ventilation with a frequency of 1–2 breaths minute⁻¹ at a tidal volume of 30 mL kg⁻¹ during anesthesia in fasted snakes.     

The effect of epidural injection speed on epidural pressure and distribution of solution in anesthetized dogs

ObjectiveTo determine the effect of injection speed on epidural pressure (EP), injection pressure (IP), epidural distribution (ED) of solution, and extent of sensory blockade (SB) during lumbosacral epidural anesthesia in dogs.Study designProspective experimental trial.AnimalsTen healthy adult Beagle dogs weighing 8.7 ± 1.6 kg.MethodsGeneral anesthesia was induced with propofol administered intravenously and maintained with isoflurane. Keeping the dogs in sternal recumbency, two spinal needles connected to electrical pressure transducers were inserted into the L6-L7 and the L7-S1 intervertebral epidural spaces for EP and IP measurements, respectively. Bupivacaine 0.5% diluted in iohexol was administered epidurally to each dog via spinal needle at L7-S1 intervertebral space, at two rates of injection (1 and 2 mL minute^?1 groups), with a 1-week washout period. Epidural distribution was verified with computed tomography, and SB was evaluated after arousal by pinching the skin with a mosquito hemostatic forceps over the vertebral dermatomes. The results were analyzed according to each injection speed, using paired t- and Wilcoxon signed-rank tests.ResultsMean ± SD of baseline EP and IP values were 2.1 ± 6.1 and 2.6 ± 7.1 mmHg, respectively. Significant differences were observed between 1 and 2 mL minute^?1 groups for peak EP (23.1 ± 8.5 and 35.0 ± 14.5 mmHg, p = 0.047) and peak IP (68.5 ± 10.7 and 144.7 ± 32.6 mmHg, p <0.001). However, the median (range) of the ED, 11.5 (4–22) and 12 (5–21) vertebrae, and SB, 3.5 (0–20) and 1 (0–20) dermatomes, values of the two groups were not related to injection speed.Conclusions and clinical relevanceThe EP profile during injection was measured by separating the injection and pressure monitoring lines. The increase in epidural injection speed increased the EP, but not the ED or the SB in dogs.     

Hyoscine‐N‐butylbromide premedication on cardiovascular variables of horses sedated with medetomidine

ObjectiveTo evaluate the effects of intravenous (IV) or intramuscular (IM) hyoscine premedication on physiologic variables following IV administration of medetomidine in horses.Study designRandomized, crossover experimental study.AnimalsEight healthy crossbred horses weighing 330 ± 39 kg and aged 7 ± 4 years.MethodsBaseline measurements of heart rate (HR), cardiac index (CI), respiratory rate, systemic vascular resistance (SVR), percentage of patients with second degree atrioventricular (2^oAV) block, mean arterial pressure (MAP), pH, and arterial partial pressures of carbon dioxide (PaCO₂) and oxygen (PaO₂) were obtained 5 minutes before administration of IV hyoscine (0.14 mg kg^?1; group HIV), IM hyoscine (0.3 mg kg^?1; group HIM), or an equal volume of physiologic saline IV (group C). Five minutes later, medetomidine (7.5 μg kg^?1) was administered IV and measurements were recorded at various time points for 130 minutes.ResultsMedetomidine induced bradycardia, 2^oAV blocks and increased SVR immediately after administration, without significant changes in CI or MAP in C. Hyoscine administration induced tachycardia and hypertension, and decreased the percentage of 2^oAV blocks induced by medetomidine. Peak HR and MAP were higher in HIV than HIM at 88 ± 18 beats minute^?1 and 241 ± 37 mmHg versus 65 ± 16 beats minute^?1 and 192 ± 38 mmHg, respectively. CI was increased significantly in HIV (p ≤ 0.05). Respiratory rate decreased significantly in all groups during the recording period. pH, PaCO₂ and PaO₂ were not significantly changed by administration of medetomidine with or without hyoscine.Conclusion and clinical relevanceHyoscine administered IV or IM before medetomidine in horses resulted in tachycardia and hypertension under the conditions of this study. The significance of these changes, and responses to other dose rates, requires further investigation.     

Minimum infusion rate and hemodynamic effects of propofol, propofol-lidocaine and propofol-lidocaine-ketamine in dogs

ObjectiveTo evaluate the effects of a constant rate infusion (CRI) of lidocaine alone or in combination with ketamine on the minimum infusion rate (MIR) of propofol in dogs and to compare the hemodynamic effects produced by propofol, propofol-lidocaine or propofol-lidocaine-ketamine anesthesia.Study designProspective, randomized cross-over experimental design.AnimalsFourteen adult mixed-breed dogs weighing 15.8 ± 3.5 kg.MethodsEight dogs were anesthetized on different occasions to determine the MIR of propofol alone and propofol in combination with lidocaine (loading dose [LD] 1.5 mg kg^?1, CRI 0.25 mg kg^?1 minute^?1) or lidocaine (LD 1.5 mg kg^?1, CRI 0.25 mg kg^?1 minute^?1) and ketamine (LD 1 mg kg^?1, CRI 0.1 mg kg^?1 minute^?1). In six other dogs, the hemodynamic effects and bispectral index (BIS) were investigated. Each animal received each treatment (propofol, propofol-lidocaine or propofol-lidocaine-ketamine) on the basis of the MIR of propofol determined in the first set of experiments.ResultsMean ± SD MIR of propofol was 0.51 ± 0.08 mg kg^?1 minute^?1. Lidocaine-ketamine significantly decreased the MIR of propofol to 0.31 ± 0.07 mg kg^?1 minute^?1 (37 ± 18% reduction), although lidocaine alone did not (0.42 ± 0.08 mg kg^?1 minute^?1, 18 ± 7% reduction). Hemodynamic effects were similar in all treatments. Compared with the conscious state, in all treatments, heart rate, cardiac index, mean arterial blood pressure, stroke index and oxygen delivery index decreased significantly, whereas systemic vascular resistance index increased. Stroke index was lower in dogs treated with propofol-lidocaine-ketamine at 30 minutes compared with propofol alone. The BIS was lower during anesthesia with propofol-lidocaine-ketamine compared to propofol alone.Conclusions and clinical relevanceLidocaine-ketamine, but not lidocaine alone, reduced the MIR of propofol in dogs. Neither lidocaine nor lidocaine in combination with ketamine attenuated cardiovascular depression produced by a continuous rate infusion of propofol.     

Development of a romifidine constant rate infusion with or without butorphanol for standing sedation of horses

ObjectiveTo determine constant rate infusion (CRI) protocols for romifidine (R) and romifidine combined with butorphanol (RB) resulting in constant sedation and romifidine plasma concentrations.Study designBlinded randomized crossover study.AnimalsTen adult research horses.MethodsPart I: After determining normal height of head above ground (HHAG = 100%), loading doses of romifidine (80 μg kg^?1) with butorphanol (RB: 18 μg kg^?1) or saline (R) were given intravenously (IV). Immediately afterwards, a butorphanol (RB: 25 μg kg^?1 hour^?1) or saline (R) CRI was administered for 2 hours. The HHAG was used as marker of sedation depth. Sedation was maintained for 2 hours by additional romifidine (20 μg kg^?1) whenever HHAG > 50%. The dose rate of romifidine (μg kg^?1 hour^?1) required to maintain sedation was calculated for both treatments. Part II: After loading doses, the romifidine CRIs derived from part I were administered in parallel to butorphanol (RB) or saline (R). Sedation and ataxia were evaluated periodically. Romifidine plasma concentrations were measured by HPLC-MS-MS at 0, 5, 10, 15, 30, 45, 60, 90, 105, and 120 minutes. Data were analyzed using paired t-test, Fisher's exact test, Wilcoxon signed rank test, and two-way anova for repeated measures (p < 0.05).ResultsThere was no significant difference in romifidine requirements (R: 30; RB: 29 μg kg^?1 hour^?1). CRI protocols leading to constant sedation were developed. Time to first additional romifidine bolus was significantly longer in RB (mean ± SD, R: 38.5 ± 13.6; RB: 50.5 ± 11.7 minutes). Constant plasma concentrations of romifidine were achieved during the second hour of CRI. Ataxia was greater when butorphanol was added.ConclusionRomifidine bolus, followed by CRI, provided constant sedation assessed by HHAG. Butorphanol was ineffective in reducing romifidine requirements in unstimulated horses, but prolonged the sedation caused by the initial romifidine bolus.Clinical relevanceBoth protocols need to be tested under clinical conditions.     

Comparison of cardiopulmonary effects of etorphine and thiafentanil administered as sole agents for immobilization of impala (Aepyceros melampus)

ObjectiveTo compare the cardiopulmonary effects of the opioids etorphine and thiafentanil for immobilization of impala.Study designTwo-way crossover, randomized study.AnimalsA group of eight adult female impala.MethodsImpala were given two treatments: 0.09 mg kg^–1 etorphine or 0.09 mg kg^–1 thiafentanil via remote dart injection. Time to recumbency, quality of immobilization and recovery were assessed. Respiratory rate, heart rate (HR), mean arterial blood pressure (MAP) and arterial blood gases were measured. A linear mixed model was used to analyse the effects of treatments, treatments over time and interactions of treatment and time (p < 0.05).ResultsTime to recumbency was significantly faster with thiafentanil (2.0 ± 0.8 minutes) than with etorphine (3.9 ± 1.6 minutes; p = 0.007). Both treatments produced bradypnoea, which was more severe at 5 minutes with thiafentanil (7 ± 4 breaths minute^–1) than with etorphine (13 ± 12 breaths minute^–1; p = 0.004). HR increased with both treatments but significantly decreased over time when etorphine (132 ± 17 to 82 ± 11 beats minute^–1) was compared with thiafentanil (113 ± 22 to 107 ± 36 beats minute^–1; p < 0.001). Both treatments caused hypertension which was more profound with thiafentanil (mean overall MAP = 140 ± 14 mmHg; p < 0.001). Hypoxaemia occurred with both treatments but was greater with thiafentanil [PaO₂ 37 ± 13 mmHg (4.9 kPa)] than with etorphine [45 ± 16 mmHg (6.0 kPa)] 5 minutes after recumbency (p < 0.001). After 30 minutes, PaO₂ increased to 59 ± 10 mmHg (7.9 kPa) with both treatments (p < 0.001).Conclusions and clinical relevanceThe shorter time to recumbency with thiafentanil may allow easier and faster retrieval in the field. However, thiafentanil caused greater hypertension, and ventilatory effects during the first 10 minutes, after administration.     

Anesthetic effects of ketamine–medetomidine–hydromorphone in dogs during high-quality,high-volume surgical sterilization program under field conditions

ObjectiveTo describe the anesthetic and adverse effects of an injectable anesthetic protocol in dogs as part of a high-volume sterilization program under field conditions in Belize.Study designProspective, observational, field study.AnimalsA total of 23 female and eight male dogs (14.2 ± 7.7 kg; age ≥ 8 weeks).MethodsUsing a volume per kg-based dose chart, dogs were administered ketamine (4.5 mg kg⁻¹), medetomidine (0.04 mg kg⁻¹) and hydromorphone (0.09 mg kg⁻¹) intramuscularly. After induction of anesthesia, an endotracheal tube was inserted and dogs were allowed spontaneous breathing in room air. Monitoring included peripheral oxygen saturation (SpO₂), mean arterial pressure (MAP), heart rate (HR), respiratory rate, rectal temperature and end-tidal carbon dioxide (Pe′CO₂). Meloxicam (0.2 mg kg⁻¹) was administered subcutaneously after surgery. Data were analyzed with linear models and chi-square tests (p < 0.05).ResultsOnset of lateral recumbency (3.4 ± 2 minutes) was rapid. Desaturation (SpO₂ < 90%) was observed at least once in 64.5% of dogs and was more frequent in large dogs (p = 0.019). Hypercapnia (Pe′CO₂ ≥ 50 mmHg; 6.7 kPa) was observed in 48.4% of dogs. MAP was 111 ± 19 mmHg, mean ± standard deviation. Hypertension (MAP ≥ 120 mmHg), bradycardia (HR ≤ 60 beats minute⁻¹) and tachycardia (HR ≥ 140 beats minute⁻¹) were observed in 45.2%, 16.1% and 3.3% of dogs, respectively. Hypotension and hypothermia were not observed. Sex was not significantly associated with any complication. Return of swallowing reflex and time to standing were 71 ± 23 and 152 ± 50 minutes after injection, respectively. Return of swallowing was significantly longer in large dogs.Conclusions and clinical relevanceAt the doses used, ketamine–medetomidine–hydromorphone was effective in dogs for high-volume sterilization. In this field setting, adverse effects included hypoventilation, hypoxemia and prolonged recovery.     

The effect of midazolam on the end-tidal concentration of isoflurane necessary to prevent movement in dogs

ObjectiveTo determine the possible additive effect of midazolam, a GABA_A agonist, on the end-tidal concentration of isoflurane that prevents movement (MAC_NM) in response to noxious stimulation.Study designRandomized cross-over experimental study.AnimalsSix healthy, adult intact male, mixed-breed dogs.MethodsAfter baseline isoflurane MAC_NM (MAC_NM-B) determination, midazolam was administered as a low (LDS), medium (MDS) or high (HDS) dose series of midazolam. Each series consisted of two dose levels, low and high. The LDS was a loading dose (Ld) of 0.2 mg kg^?1 and constant rate infusion (CRI) (2.5 μg kg^?1 minute^?1) (LDL), followed by an Ld (0.4 mg kg^?1) and CRI (5 μg kg^?1 minute^?1) (LDH). The MDS was an Ld (0.8 mg kg^?1) and CRI (10 μg kg^?1 minute^?1) (MDL) followed by an Ld (1.6 mg kg^?1) and CRI (20 μg kg^?1 minute^?1) (MDH). The HDS was an Ld (3.2 mg kg^?1) and CRI (40 μg kg^?1 minute^?1) (HDL) followed by an Ld (6.4 mg kg^?1) and CRI (80 μg kg^?1 minute^?1) (HDH). MAC_NM was re-determined after each dose in each series (MAC_NM-T).ResultsThe median MAC_NM-B was 1.42. MAC_NM-B did not differ among groups (p >0.05). Percentage reduction in MAC_NM was significantly less in the LDS (11 ± 5%) compared with MDS (30 ± 5%) and HDS (32 ± 5%). There was a weak correlation between the plasma midazolam concentration and percentage MAC_NM reduction (r = 0.36).Conclusion and clinical relevanceMidazolam doses in the range of 10–80 μg kg^?1 minute^?1 significantly reduced the isoflurane MAC_NM. However, doses greater than 10 μg kg^?1 minute^?1 did not further decrease MAC_NM indicating a ceiling effect.     

Cardiovascular effects of intravenous vatinoxan (MK-467) in medetomidine–tiletamine–zolazepam anaesthetised red deer (Cervus elaphus)

ObjectiveTo determine the effect of intravenous vatinoxan administration on bradycardia, hypertension and level of anaesthesia induced by medetomidine–tiletamine–zolazepam in red deer (Cervus elaphus).Study design and animalsA total of 10 healthy red deer were included in a randomised, controlled, experimental, crossover study.MethodsDeer were administered a combination of 0.1 mg kg^–1 medetomidine hydrochloride and 2.5 mg kg^–1 tiletamine–zolazepam intramuscularly, followed by 0.1 mg kg^–1 vatinoxan hydrochloride or equivalent volume of saline intravenously (IV) 35 minutes after anaesthetic induction. Heart rate (HR), mean arterial blood pressure (MAP), respiration rate (f_R), end-tidal CO₂ (Pe′CO₂), arterial oxygen saturation (SpO₂), rectal temperature (RT) and level of anaesthesia were assessed before saline/vatinoxan administration (baseline) and at intervals for 25 minutes thereafter. Differences within treatments (change from baseline) and between treatments were analysed with linear mixed effect models (p < 0.05).ResultsMaximal (81 ± 10 beats minute^–1) HR occurred 90 seconds after vatinoxan injection and remained significantly above baseline (42 ± 4 beats minute^–1) for 15 minutes. MAP significantly decreased from baseline (122 ± 10 mmHg) to a minimum MAP of 83 ± 6 mmHg 60 seconds after vatinoxan and remained below baseline until end of anaesthesia. HR remained unchanged from baseline (43 ± 5 beats minute^–1) with the saline treatment, whereas MAP decreased significantly (112 ± 16 mmHg) from baseline after 20 minutes. Pe′CO₂, f_R and SpO₂ showed no significant differences between treatments, whereas RT decreased significantly 25 minutes after vatinoxan. Level of anaesthesia was not significantly influenced by vatinoxan.Conclusions and clinical relevanceVatinoxan reversed hypertension and bradycardia induced by medetomidine without causing hypotension or affecting the level of anaesthesia in red deer. However, the effect on HR subsided 15 minutes after vatinoxan IV administration. Vatinoxan has the potential to reduce anaesthetic side effects in non-domestic ruminants immobilised with medetomidine–tiletamine–zolazepam.     

Effect of intravenous propofol and remifentanil on heart rate, blood pressure and nociceptive response in acepromazine premedicated dogs

ObjectiveTo investigate the cardiorespiratory, nociceptive and endocrine effects of the combination of propofol and remifentanil, in dogs sedated with acepromazine.Study designProspective randomized, blinded, cross-over experimental trial.AnimalsTwelve healthy adult female cross-breed dogs, mean weight 18.4 ± 2.3 kg.MethodsDogs were sedated with intravenous (IV) acepromazine (0.05 mg kg^?1) followed by induction of anesthesia with IV propofol (5 mg kg^?1). Anesthesia was maintained with IV propofol (0.2 mg kg^?1 minute^?1) and remifentanil, infused as follows: R1, 0.125 μg kg^?1 minute^?1; R2, 0.25 μg kg^?1 minute^?1; and R3, 0.5 μg kg^?1 minute^?1. The same dogs were administered each dose of remifentanil at 1-week intervals. Heart rate (HR), mean arterial pressure (MAP), respiratory rate (f_R), end tidal CO₂ (Pe′CO₂), arterial hemoglobin O₂ saturation, blood gases, and rectal temperature were measured before induction, and 5, 15, 30, 45, 60, 75, 90, and 120 minutes after beginning the infusion. Nociceptive response was investigated by electrical stimulus (50 V, 5 Hz and 10 ms). Blood samples were collected for plasma cortisol measurements. Statistical analysis was performed by anova (p < 0.05).ResultsIn all treatments, HR decreased during anesthesia with increasing doses of remifentanil, and increased significantly immediately after the end of infusion. MAP remained stable during anesthesia (72–98 mmHg). Antinociception was proportional to the remifentanil infusion dose, and was considered satisfactory only with R2 and R3. Plasma cortisol concentration decreased during anesthesia in all treatments. Recovery was smooth and fast in all dogs.Conclusions and clinical relevanceInfusion of 0.25–0.5 μg kg^?1 minute^?1 remifentanil combined with 0.2 mg kg^?1 minute^?1 propofol produced little effect on arterial blood pressure and led to a good recovery. The analgesia produced was sufficient to control the nociceptive response applied by electrical stimulation, suggesting that it may be appropriate for performing surgery.     

Epidural ketamine in the dromedary camel

ObjectiveTo evaluate the clinical and physiological effects of epidural injection of ketamine in camels.Study designRandomized prospective study.AnimalsTen healthy immature male dromedary camels.MethodsKetamine was administered epidurally at doses of 1 and 2 mg kg^?1 (five animals in each treatment). The drug was injected into the first intercoccygeal epidural space. Anti-nociception, sedation, ataxia, and effect on cardiopulmonary, rectal temperature and some selected haematological parameters were recorded at different intervals before (baseline) and after the drug administration. Data were analyzed by anova or U Mann–Whitney tests, as relevant and significance was taken as p < 0.05.ResultsEpidural ketamine at the 2 mg kg^?1 dose produced complete anti-nociception in the tail, anus and perineum, whilst the 1 mg kg^?1 dose produced complete anti-nociception only in the tail. Epidural ketamine resulted in mild to moderate sedation at the 1 mg kg^?1 dose and deep sedation at the 2 mg kg^?1 dose. Ataxia was observed in all test subjects and was severe, resulting in recumbency, in the 2 mg kg^?1 group. Respiratory rate and rectal temperature did not change significantly after injection of either treatment. Following epidural injection of 2 mg kg^?1 of ketamine, heart rate increased significantly from the pre-injection baseline of 55 ± 2 to 76 ± 4 (mean ± SD) beats minute^?1, but after the lower dose changes were not significant. The only significant changes in measured haematologic parameters were decreases in total erythrocyte count at 45 minutes and total leukocyte count from 45–75 minutes, in the 2 mg kg^?1 group.ConclusionEpidural ketamine injection was associated with caudal anti-nociception, sedation and ataxia in the dromedary camels; the intensity and duration of which was dose dependant.Clinical relevanceNeither of the doses of epidural ketamine injection in our study was applicable for standing surgical procedures in dromedary camels.