Pharmacokinetics of enrofloxacin after intravenous,intramuscular and oral administration in houbara bustard (Chlamydotis undulata macqueenii)

The in-vitro activity of enrofloxacin against 117 strains of bacteria isolated from bustards was determined. Minimum inhibitory concentrations for 72% of the Proteus spp., E. coli, Salmonella spp. and Klebsiella spp. (n = 61) and for 48% of the Streptococci spp. and Staphylococci spp. (n = 31) were 0.5 μ g/mL. The minimum inhibitory concentration (MIC) of 76% of Pseudomonas spp. (n = 25) was 2 μg/mL. Fourteen strains were resistant to concentrations 128 μg/mL. The elimination half-lives (t½ elim β) (mean± SEM) of 10 mg/kg enrofloxacin in eight houbara bustards (Chlamydotis undulata) were 6.80± 0.79, 6.39± 1.49 and 5.63± 0.54 h after oral (p.o.), intramuscular (i.m.) and intravenous (i.v.) administration, respectively. Enrofloxacin was rapidly absorbed from the bustard gastro-intestinal tract and maximum plasma concentrations of 1.84± 0.16 μg/mL were achieved after 0.66± 0.05 h. Maximum plasma concentration after i.m. administration of 10 mg/kg was 2.75± 0.11 μg/mL at 1.72± 0.19 h. Maximum plasma concentration after i.m. administration of 15 mg/kg in two birds was 4.86 μg/mL. Bioavailability was 97.3± 13.7% and 62.7± 11.1% after i.m. and oral administration, respectively. Plasma concentrations of enrofloxacin 0.5 μg/mL were maintained for at least 12 h for all routes at 10 mg/kg and for 24 h after i.m. administration at 15 mg/kg. Plasma enrofloxacin concentrations were monitored during the first 3 days of treatment in five houbara bustards and kori bustards (Ardeotis kori) with bacterial infections receiving a single daily i.m. injection of 10 mg/kg for 3 days. The mean plasma enrofloxacin concentrations in the clinical cases at 27 and 51 h (3.69 and 3.86 μg/mL) and at 48 h (0.70 μg/mL) were significantly higher compared with the 3 h and 24 h time intervals from clinically normal birds. The maximum plasma concentration (C_max)/MIC ratio was ranked i.v. (10/mg/kg) > i.m. (15 mg/kg) > i.m. (10 mg/kg) > oral (10 mg/kg), but it was only higher than 8:1 for i.v and i.m. administrations of enrofloxacin at 10 mg/kg and 15 mg/kg, respectively, against a low MIC (0.5 μg/mL). A dosage regimen of 10 mg/kg repeated every 12 h, or 15 mg/kg repeated every 24 h, would be expected to give blood concentrations above 0.5 μg/mL and hence provide therapeutic response in the bustard against a wide range of bacterial infections.     

The influence of atipamezole on the cardiovascular effects of detomidine in horses

The reversal of the cardiovascular effects of the α₂-adrenoceptor agonist detomidine by the α₂-antagonist atipamezole was studied. Nine horses were given detomidine 20 μg/kg iv. On a separate occasion they were given atipamezole 100 μg/kg iv 15 mins after the detomidine injection. Blood gas tensions were measured and clinical signs of sedation were also observed. Bradycardia and the frequency of heart blocks induced by detomidine were reduced after atipamezole and blood pressure decreased. These reversal effects of atipamezole were of short duration (a few minutes) at the dose level tested. Two of the nine horses exhibited premature depolarisations after administration of detomidine, but not after atipamezole injection. PaO₂ decreased and PaCO₂ increased slightly after detomidine injection, but the arterial pH was within reference values or slightly elevated. Administration of atipamezole did not alter these values. Base excess rose after detomidine, and it decreased more quickly towards the baseline level, when the horses were given detomidine alone. No clinical adverse effects were seen from the administration of atipamezole. Atipamezole may be beneficial, if detomidine-induced bradycardia needs to be reversed in horses.     

Medetomidine/ketamine sedation in calves and its reversal with atipamezole

Atipamezole was used to reverse the sedation induced in calves by medetomidine/ketamine. Thirteen claves subjected to umbilical surgery received medetomidine 20 μg/kg bodyweight (bwt) and ketamine 0.5 mg/kg bwt intravenously (iv) from a mixture of the drugs in one syringe. Atipamezole was given at doses of 20 to 60 μg/kg iv and intramuscularly (im) to the calves at the end of the operation. Following the administration of medetomidine and ketamine, PaCO₂ increased whereas pH, PaO₂ and heart rate decreased. Reversing the effects of medetomidine with atipamezole did not cause undesirable effects; recovery was rapid and smooth, most of the animals reached a standing position within 1 to 3 mins after the atipamezole injection.     

A comparison of the antinociceptive effects of xylazine, detomidine and romifidine on experimental pain in horses

Objective To study the analgesic potency of the α₂‐agonist romifidine in the horse using both an electrical current and a mechanical pressure model for nociceptive threshold testing. In addition, a comparison was made with doses of detomidine and xylazine that produce equivalent degrees of sedation. Study design Randomized, placebo‐controlled, blinded cross‐over study. Animals Six adult Swiss warmblood horses, one mare and five geldings, weighing from 530 to 650 kg and aged 6–15 years. Methods Nociceptive thresholds were measured using an electrical stimulus applied to the coronary band and using a pneumatically operated pin pressing on the cannon bone. Measurements were made immediately before and every 15 minutes for 2 hours after IV injection of the test substances. Lifting of the foot indicated the test end point. Results The three α₂‐agonists caused a temporary increase in nociceptive thresholds with a maximal effect within 15 minutes and a return to baseline levels within 1 hour. Using electrical current testing nociceptive thresholds were significantly different from placebo (mean ± SD) for detomidine at 15 minutes (from control 5.8 ± 0.9 to 23.3 ± 3.9 mA, p = 0.0066) and 30 minutes (from control 6.6 ± 1.1 to 18.8 ± 3.3 mA, p = 0.0091). The difference was significant for romifidine at 15 minutes only (from control 5.8 ± 0.9 to 18.7 ± 3.8 mA, p = 0.0066). With mechanical pressure testing nociceptive thresholds were significantly different from control for detomidine at 15 minutes (from 3.2 ± 0.2 to 6.2 ± 0.5 N, p = 0.00076) and 30 minutes (from 3.2 ± 0.7 to 5.7 ± 0.8 N, p = 0.0167). The difference was significant for xylazine at 15 minutes (from control 3.2 ± 0.2 to 5.6 ± 0.7 N, p = 0.0079). At 15 minutes the order of magnitude of the measured antinociceptive effect was significantly different between the two pain tests for both romifidine and detomidine, but not for xylazine. For romifidine, the increase of mean thresholds compared to placebo was 4.0 ± 1.3 times placebo levels with the electrical current test compared to 1.3 ± 0.3 times for the mechanical pressure test (p = 0.037). For detomidine, the increase of mean thresholds compared to placebo was 5.4 ± 1.7 times control levels with the electrical current test compared to 2.0 ± 0.2 times for the mechanical pressure test (p = 0.040). This represents a 2.7 (romifidine) and 3.4 times (detomidine) greater increase in thresholds using electrical current testing compared to the use of mechanical pressure testing. Conclusion and clinical relevance This study demonstrates the analgesic potential of α₂‐agonists in the horse for somatic pain and that they can have quantitatively different antinociceptive effects according to the antinociceptive test used.     

Effects of selective α2‐adrenergic receptor agonists on electrical field‐stimulated contractions of isolated bronchi in horses

We investigated the effects of different selective α₂‐adrenergic receptor (AR ) agonists (detomidine, medetomidine, xylazine, and brimonidine) on the contractions of horse‐isolated bronchi induced by electrical field stimulation (EFS ) and by carbachol. No effects were observed on the contraction induced by carbachol, while α₂‐AR agonists reduced EFS ‐evoked contractions in a concentration‐related fashion. The rank order of potency (pD ₂) was brimonidine (7.40 ± 0.20) >medetomidine (7.09 ± 0.24) >detomidine (6.13 ± 0.55) >xylazine (4.59 ± 0.16). The maximal effects (E_max) were ?56.3% ± 6.3%, ?40.4% ± 6.9%, ?48.6% ± 9.9%, and ?72.7% ± 12.7% for brimonidine, medetomidine, detomidine, and xylazine, respectively. Adrenergic block by guanethidine enhanced the potency (8.10 ± 0.05, 7.30 ± 0.15, 6.83 ± 0.41, and 5.40 ± 0.22) and the efficacy (?95.2% ± 0.7%, ?45.2% ± 11.7%, ?58.5% ± 9.8%, and ?97.9% ± 0.6%) of brimonidine, medetomidine, detomidine, and xylazine, respectively. Selective α₂‐AR antagonist, atipamezole, competitively antagonized the inhibition of EFS ‐evoked contractions induced by all agonists except xylazine. These results suggest the existence of presynaptic α₂‐AR s on cholinergic neurons, negatively regulating the release of acetylcholine in horse bronchial muscle, and that α₂‐AR agonists may be beneficial against vagally mediated bronchoconstriction.     

Sedative effects of romifidine in the dog

The sedative and physiological effects of intravenous romifidine at 0, 20, 40, 80 and 120 μg/kg were investigated in five clinically normal adult male beagle dogs in a blind study using a Latin square design. Following the injection of romifidine, the dogs became ataxic and stood with a wide-based stance, they exhibited signs of skeletal muscle relaxation and their heads were lowered. All the dogs became recumbent and there was a reduction in the heart and respiratory rates. Increasing the dose from 20 to 40 μg/kg, or higher, produced a significant reduction in heart rate. There was an increase in the sedation score following even low doses of romifidine, and although measures of sedation showed no differences among romifidine doses, subjectively, the higher doses produced a more consistent effect. Dogs given lower doses of romifidine regained a standing position more rapidly than following the higher doses, although this effect was not significantly different. A second blind study compared the sedative effects of intravenous romifidine, at 40 and 80 μg/kg, with mede-tomidine at 10 μg/kg in six adult beagles. The cardiopulmonary and sedative effects were not significantly different between all regimens, although medetomidine at 10 μg/kg appeared to be intermediate in effect between romifidine at 40 and 80 μ/kg. The sedative and physiological effects of romifidine in dogs appear to be similar to other α₂-adrenoceptor agonists. Intravenous administration provided sedation which might be clinically useful.     

Cardiovascular effects of medetomidine-ketamine anaesthesia in sheep, with and without 100% oxygen, and its reversal with atipamezole.

The cardiovascular effects of intravenously (iv) administered medetomidine 20 μg/kg bodyweight (bwt) and ketamine (2 mg/kgbwt), with and without 100% inspired oxygen, were investigated in six domestic sheep. A second dose of medetomidine and ketamine was administered iv, at dose 10 μg/kg bwt and 1 mg/kg bwt respectively, 25 minutes after the initial injection. Heart rate, PaO₂ pH and haemoglobin saturation decreased whereas PaCO₂ and base excess increased post-injection. Transient hypertension and an increase in respiration rate were evident within the first 10 minutes of anaesthesia. Significant hypoxaemia (P<0.01) developed in sheep breathing room air. Inspired 100% oxygen improved PaO₂ (but the difference was not significant), and improved haemoglobin saturation significantly (P<0.05), however, this effect varied between individuals. One sheep breathing room air suffered a cardiac arrest immediately post-injection and had to be resuscitated. Atipamezole 125 μg/kg given intramuscularly 45 minutes after the initial injection rapidly reversed the effects of medetomidine. Recovery times did not significantly differ although time to extubation and standing tended to be longer in sheep breathing room air compared to the sheep breathing 100% oxygen. The quality of the recovery did not differ.     

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.     

Effect of sedation with detomidine and butorphanol on pulmonary gas exchange in the horse

Background

Sedation with α₂-agonists in the horse is reported to be accompanied by impairment of arterial oxygenation. The present study was undertaken to investigate pulmonary gas exchange using the Multiple Inert Gas Elimination Technique (MIGET), during sedation with the α₂-agonist detomidine alone and in combination with the opioid butorphanol.

Methods

Seven Standardbred trotter horses aged 3–7 years and weighing 380–520 kg, were studied. The protocol consisted of three consecutive measurements; in the unsedated horse, after intravenous administration of detomidine (0.02 mg/kg) and after subsequent butorphanol administration (0.025 mg/kg). Pulmonary function and haemodynamic effects were investigated. The distribution of ventilation-perfusion ratios (V_A/Q) was estimated with MIGET.

Results

During detomidine sedation, arterial oxygen tension (PaO₂) decreased (12.8 ± 0.7 to 10.8 ± 1.2 kPa) and arterial carbon dioxide tension (PaCO₂) increased (5.9 ± 0.3 to 6.1 ± 0.2 kPa) compared to measurements in the unsedated horse. Mismatch between ventilation and perfusion in the lungs was evident, but no increase in intrapulmonary shunt could be detected. Respiratory rate and minute ventilation did not change. Heart rate and cardiac output decreased, while pulmonary and systemic blood pressure and vascular resistance increased. Addition of butorphanol resulted in a significant decrease in ventilation and increase in PaCO₂. Alveolar-arterial oxygen content difference P(A-a)O₂ remained impaired after butorphanol administration, the V_A/Q distribution improved as the decreased ventilation and persistent low blood flow was well matched. Also after subsequent butorphanol no increase in intrapulmonary shunt was evident.

Conclusion

The results of the present study suggest that both pulmonary and cardiovascular factors contribute to the impaired pulmonary gas exchange during detomidine and butorphanol sedation in the horse.     

Behavioural and cardiovascular effects of medetomidine constant rate infusion compared with detomidine for standing sedation in horses

ObjectiveTo compare the efficacy of a medetomidine constant rate infusion (CRI) with a detomidine CRI for standing sedation in horses undergoing high dose rate brachytherapy.Study designRandomized, controlled, crossover, blinded clinical trial.AnimalsA total of 50 horses with owner consent, excluding stallions.MethodsEach horse was sedated with intravenous acepromazine (0.02 mg kg^–1), followed by an α₂-adrenoceptor agonist 30 minutes later and then by butorphanol (0.1 mg kg^–1) 5 minutes later. A CRI of the same α₂-adrenoceptor agonist was started 10 minutes after butorphanol administration and maintained for the treatment duration. Treatments were given 1 week apart. Each horse was sedated with detomidine (bolus dose, 10 μg kg^–1; CRI, 6 μg kg^–1 hour^–1) or medetomidine (bolus dose, 5 μg kg^–1; CRI, 3.5 μg kg^–1 hour^–1). If sedation was inadequate, a quarter of the initial bolus of the α₂-adrenoceptor agonist was administered. Heart rate (HR) was measured via electrocardiography, and sedation and behaviour evaluated using a previously published scale. Between treatments, behaviour scores were compared using a Wilcoxon signed-rank test, frequencies of arrhythmias with chi-square tests, and HR with two-tailed paired t tests. A p value <0.05 indicated statistical significance.ResultsTotal treatment time for medetomidine was longer than that for detomidine (p = 0.04), and ear movements during medetomidine sedation were more numerous than those during detomidine sedation (p = 0.03), suggesting there may be a subtle difference in the depth of sedation. No significant differences in HR were found between treatments (p ≥ 0.09). Several horses had arrhythmias, with no difference in their frequency between the two infusions.Conclusions and clinical relevanceMedetomidine at this dose rate may produce less sedation than detomidine. Further studies are required to evaluate any clinical advantages to either drug, or whether a different CRI may be more appropriate.     

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.     

A review of clinical approaches to antagonism of alpha2‐adrenoreceptor agonists in the horse

Alpha₂‐adrenoceptor agonists xylazine, romifidine, detomidine and, in some cases, medetomidine and dexmedetomidine, are fundamental drugs used in equine practice. There are situations where the undesirable pharmacodynamic effects (ataxia, prolonged sedation, bradycardia and ileus) or accidental overdose of these drugs may need to be antagonised. The α₂‐adrenoceptor antagonists tolazoline, yohimbine and atipamezole can be used to antagonise undesirable effects. However, despite being effective, α₂‐adrenoceptor antagonists are also not without undesirable pharmacodynamic effects. Excitement, muscle trembling and triggered inappropriate stress responses are a few of the more serious undesirable effects. Horses demonstrate a variable response to the antagonists thus recommending dose rates become fraught with difficulty. It is therefore recommended that the α₂‐adrenoceptor antagonist should be titrated to the desired clinical effect. Consequently, other reversal agents, such as anticholinergics (atropine, glycopyrrolate and hyoscine), have been administered for the treatment of α₂‐adrenoceptor agonist‐induced bradycardia. Anticholinergics cannot be recommended for routine use in horses due to the undesirable cardiovascular effects and potentiation of α₂‐adrenoceptor agonist‐induced gastrointestinal hypomotility. Novel peripheral acting α₂‐adrenoceptor antagonists, such as MK‐467, are currently under scrutiny in veterinary anaesthesia in an effort to antagonise the undesirable effects of α₂‐adrenoceptor agonists without compromising on the level of sedation. This review examines the current literature on the α₂‐adrenoceptor antagonists used in horses and makes recommendations on how to use these drugs safely in an attempt to prevent undesirable pharmacodynamic effects.     

Pain control in horses: What do we really know?

Currently, approaches to pain control in horses are a mixture of art and science. Recognition of overt pain behaviours, such as rolling, kicking at the abdomen, flank watching, lameness or blepharospasm, may be obvious; subtle signs of pain can include changes in facial expression or head position, location in the stall and response to palpation or human interaction. Nonsteroidal anti‐inflammatory drugs (i.e. phenylbutazone, flunixin meglumine and firocoxib), opioids (i.e. butorphanol, morphine and buprenorphine) and α₂‐adrenergic agonists (i.e. xylazine, detomidine, romifidine and medetomidine) are the most commonly used therapeutic options. Multimodal therapy using constant‐rate infusions of lidocaine, ketamine and/or butorphanol has gained popularity for severe pain in hospitalised cases. Drugs targeting neuropathic pain, such as gabapentin, are increasingly used for conditions such as laminitis. Optimal strategies for management of pain are based upon severity and chronicity, including special considerations for use of intra‐articular or epidural delivery and therapy in foals. Strategies that aim to mitigate adverse effects associated with use of various analgesic agents are briefly discussed.     

Comparison of the effects of the alpha-2 agonists detomidine, romifidine and xylazine on nociceptive withdrawal reflex and temporal summation in horses

ObjectiveTo evaluate and compare the antinociceptive effects of the three alpha-2 agonists, detomidine, romifidine and xylazine at doses considered equipotent for sedation, using the nociceptive withdrawal reflex (NWR) and temporal summation model in standing horses.Study designProspective, blinded, randomized cross-over study.AnimalsTen healthy adult horses weighing 527–645 kg and aged 11–21 years old.MethodsElectrical stimulation was applied to the digital nerves to evoke NWR and temporal summation in the left thoracic limb and pelvic limb of each horse. Electromyographic reflex activity was recorded from the common digital extensor and the cranial tibial muscles. After baseline measurements a single bolus dose of detomidine, 0.02 mg kg^?1, romifidine 0.08 mg kg^?1, or xylazine, 1 mg kg^?1, was administered intravenously (IV). Determinations of NWR and temporal summation thresholds were repeated at 10, 20, 30, 40, 60, 70, 90, 100, 120 and 130 minutes after test-drug administration alternating the thoracic limb and the pelvic limb. Depth of sedation was assessed before measurements at each time point. Behavioural reaction was observed and recorded following each stimulation.ResultsThe administration of detomidine, romifidine and xylazine significantly increased the current intensities necessary to evoke NWR and temporal summation in thoracic limbs and pelvic limbs of all horses compared with baseline. Xylazine increased NWR thresholds over baseline values for 60 minutes, while detomidine and romifidine increased NWR thresholds over baseline for 100 and 120 minutes, respectively. Temporal summation thresholds were significantly increased for 40, 70 and 130 minutes after xylazine, detomidine and romifidine, respectively.Conclusions and clinical relevanceDetomidine, romifidine and xylazine, administered IV at doses considered equipotent for sedation, significantly increased NWR and temporal summation thresholds, used as a measure of antinociceptive activity. The extent of maximal increase of NWR and temporal summation thresholds was comparable, while the duration of action was drug-specific.     

Effects of intravenous terbutaline on heart rate,arterial pressure and blood gases in anesthetized horses breathing air

Objective

To investigate the effects of intravenous (IV) administration of terbutaline on PaO₂, PaCO₂, pH, heart rate (HR) and arterial pressures in healthy, laterally recumbent horses breathing ambient air under total intravenous anesthesia (TIVA).

Evaluation of lung ventilation distribution using electrical impedance tomography in standing sedated horses with capnoperitoneum

ObjectiveTo determine changes in distribution of lung ventilation with increasing intra-abdominal pressure (IAP) from carbon dioxide (CO₂) insufflation in standing sedated horses.Study designProspective experimental study.AnimalsA group of six healthy adult horses.MethodsEach horse was sedated with acepromazine, detomidine and butorphanol and sedation maintained with a detomidine infusion. The horse was restrained in a stocks system and a 32 electrode electrical impedance tomography (EIT) belt was wrapped around the thorax at the fifth–sixth intercostal space. EIT images and arterial blood samples for PaO₂ and PaCO₂, pH and lactate concentration were obtained during capnoperitoneum at 0 (baseline A), 5, 8 and 12 mmHg as IAP increased and at 8, 5, 0 (baseline B) mmHg as IAP decreased. At each IAP, after a 2 minute stabilization period, EIT images were recorded for ≥ 2 minutes to obtain five consecutive breaths. Statistical analysis was performed using anova for repeated measures with Geisser-Greenhouse correction and a Tukey’s multiple comparison test for parametric data. The relationship between PaO₂ and the center of ventilation in the ventral-dorsal (CoV-VD) and right-left (CoV-RL) directions or total impedance change as a surrogate for tidal volume (ΔZV_T) were tested using linear regression analysis. Significance was assumed when p ≤ 0.05.ResultsThere were no significant changes in CoV-VD, CoV-RL, PaO₂, PaCO₂, lactate concentration, pH, heart rate and respiratory rate with targeted IAP. There was a significant decrease in ΔZV_T compared with baseline A at 5 mmHg IAP as IAP was increased.Conclusions and clinical relevanceCapnoperitoneum causes a significant decrease in ΔZV_T in standing sedated horses with increasing IAP.     

Effects of α2-adrenergic drugs on blood platelets in sheep

Xylazine (0.2 mg/kg, iv) alone or preceded by atipame-zole (0.125 μg/kg, iv) or by aspirin (10 μg/kg, iv) was administered to 18 sheep. Medetomidine (60 μg/kg, iv) was also administered to 12 sheep. Xylazine, but not medetomidine, significantly reduced the number of platelets. Both atipamezole and aspirin prevented this reduction. It was concluded that α₂-agonists would seem to produce platelet aggregation that may contribute to the development of the respiratory changes that follow the administration of α₂-agonists in sheep, but probably not always to a degree that could result in a significant decrease in the number of circulating platelets.     

Pulsed delivery of inhaled nitric oxide counteracts hypoxaemia during 2.5 hours of inhalation anaesthesia in dorsally recumbent horses

Objective The study aimed to investigate the effect of varying pulse lengths of inhaled nitric oxide (iNO), and 2.5 hours of continuous pulse‐delivered iNO on pulmonary gas exchange in anaesthetized horses. Study Design Experimental study. Animals Six Standardbred horses. Methods Horses received acepromazine, detomidine, guaifenesin, thiopentone and isoflurane in oxygen, were positioned in dorsal recumbency and were breathing spontaneously. iNO was on average pulsed during the first 20, 30, 43 or 73% of the inspiration in 15 minute steps. The pulse length that corresponded to the highest (peak) partial pressure of arterial oxygen (PaO₂) in the individual horses was determined and delivered for a further 1.5 hours. Data measured or calculated included arterial and mixed venous partial pressures of O₂ and CO₂, heart rate, respiratory rate, expired minute ventilation, pulmonary and systemic arterial mean pressures, cardiac output and venous admixture. Data (mean ± SD) was analysed using anova with p < 0.05 considered significant. Results Although the pulse length of iNO that corresponded to peak PaO₂ varied between horses, administration of all pulse lengths of iNO increased PaO₂ compared to baseline. The shortest pulse lengths that resulted in the peak PaO₂ were 30 and 43% of the inspiration. Administration of iNO increased PaO₂ (12.6 ± 4.1 kPa [95 ± 31 mmHg] at baseline to a range of 23.0 ± 8.4 to 25.3 ± 9.0 kPa [173 to 190 mmHg]) and PaCO₂ (8.5 ± 1.2 kPa [64 ± 9 mmHg] to 9.8 ± 1.5 kPa [73 ± 11 mmHg]) and decreased venous admixture from 32 ± 6% to 25 ± 6%. The increase in PaO₂ and decrease in venous admixture was sustained for the entire 2.5 hours of iNO delivery. Conclusions The improvement in arterial oxygenation during pulsed delivery of iNO was significant and sustained throughout 2.5 hours of anaesthesia. Clinical relevance Pulsed iNO potentially could be used clinically to counteract hypoxemia in anaesthetized horses.