Hemodynamic Effects of Medetomidine in the Dog: A Dose Titration Study

Objective —To characterize the hemodynamic effects of medetomidine administered intravenously at doses ranging from 1 to 20 μg/kg, and to determine whether these effects are dose dependent. Study Design —Prospective randomized multidose trial. Animals —Twenty-five clinically normal male beagles (5 groups of 5), aged 1 to 4 years and weighing 13.5 ±1.7 kg. Methods —Medetomidine, at a dose of 1, 2, 5, 10, or 20 μg/kg, was administered intravenously at time 0. Heart rate, arterial pressure, central venous pressure, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, body temperature, cardiac output, and packed cell volume were measured immediately before and at selected times after medetomidine administration (3, 7, 10, 20, 30, 40, 50, and 60 minutes in all groups, at 90 minutes for the 10 and 20 μg/kg groups, and at 120 minutes for the highest dose). Cardiac index, stroke index, rate-pressure product, systemic vascular resistance index, pulmonary vascular resistance index, and left and right ventricular stroke work indices were calculated. The degree of sedation was subjectively scored by an observer who was blinded to the treatment used. Results —Heart rate, rate-pressure product, cardiac index, and left and right ventricular stroke work indices decreased below baseline values. Central venous pressure and systemic vascular resistance index increased above baseline measurements. Except in the 2 μg/kg group, after an initial and short lasting increase, a prolonged decrease in arterial pressure was observed. Conclusions —Hemodynamic changes were observed with the intravenous (IV) administration of medetomidine, at any dose. However, the two lowest doses (1 and 2 μg/kg) produced less cardiovascular depression. Clinical Relevance —Medetomidine is an alpha-2 adrenoceptor agonist widely used in dogs, producing sedation, analgesia and cardiovascular depression. When using IV medetomidine, a reduction of the recommended dosage (ie, ±30 to 40 μg/kg) by up to 6 times did not significantly influence the cardiovascular effects.     

Hemodynamic Effects of Intravenous Midazolam-Xylazine-Butorphanol in Dogs

The hemodynamic effects of a mixture of midazolam (1.0 mg/kg), xylazine (0.44 mg/kg), and butorphanol (0.1 mg/kg) were evaluated in six adult dogs. The dogs were anesthetized with isoflurane for instrumentation. As the dogs returned to consciousness, baseline values were recorded and the midazolam-xylazine-butorphanol mixture and glycopyrrolate (0.01 mg/kg) were administered intravenously (IV). Hemodynamic data were recorded 3, 10, 20, 30, 40, 50, and 60 minutes after injection. Mean arterial pressure (AP), mean pulmonary arterial pressure (PAP), heart rate (HR), rate-pressure product (RPP), mean pulmonary capillary wedge pressure (PCWP), systemic vascular resistance (SVR), and right ventricular stroke work index (RVSWI) were increased significantly above baseline values. Cardiac output (CO), stroke volume (SV), cardiac index (CI), stroke index (SI), mean central venous pressure (CVP), and left ventricular stroke work index (LVSWI) were decreased significantly below baseline values. When administered IV at the dosages used in this study, midazolam-xylazine-butorphanol-glycopyrrolate induced profound acute alterations in several critical hemodynamic variables.     

Cardiovascular effects of vasopressors in halothane-anesthetized dogs before and after hemorrhage

Exogenously administered vasopressors (sympathomimetics) were evaluated in halothane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and halothane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure (SAP), heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Dobutamine administered at the low dose before hemorrhage increased SAP and dP/dT. At the high and medium dose, dobutamine significantly increased CI, dP/dT, and SAP, with no significant change in HR or SVR. The medium dose of epinephrine was the most effective dose of epinephrine at increasing key variables (CI, SI, dP/dT). The response of CI and SI to this dose was not significantly different from the changes seen with high-dose administration of dobutamine. The dP/dT was significantly lower with epinephrine than with dobutamine, and SVR and HR were unchanged with epinephrine, except at the low dose, which decreased SVR.     

Cardiovascular effects of vasopressors in isoflurane-anesthetized dogs before and after hemorrhage

Exogenously administered vasopressors (sympathomimetics) were evaluated in isoflurane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and isoflurane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure, heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Before hemorrhage, administration of high doses of dobutamine and medium and high doses of epinephrine were equally effective at increasing CI and SI. The dP/dT was increased to the greatest degree by administration of high doses of dobutamine. Administration of the low dose of dobutamine increased dP/dT, whereas administration of the low dose of epinephrine increased CI, HR, and SI, and decreased SVR. The HR and SVR were not increased by administration of any dose of dobutamine or of the medium and high doses of epinephrine. However, methoxamine increased SVR and decreased HR. Methoxamine decreased CI, SI, and dP/dT, but increased systemic arterial pressure to the same degree as that attributed to administration of high doses of dobutamine and epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiopulmonary effects of romifidine/ketamine or xylazine/ketamine when used for short duration anesthesia in the horse

The cardiovascular changes associated with anesthesia induced and maintained with romifidine/ketamine versus xylazine/ ketamine were compared using 6 horses in a cross over design. Anesthesia was induced and maintained with romifidine (100 microg/kg, IV)/ketamine (2.0 mg/kg, IV) and ketamine (0.1 mg/kg/min, IV), respectively, in horses assigned to the romifidine/ ketamine group. Horses assigned to the xylazine/ketamine group had anesthesia induced and maintained with xylazine (1.0 mg/kg, IV)/ketamine (2.0 mg/kg, IV) and a combination of xylazine (0.05 mg/kg/min, IV) and ketamine (0.1 mg/kg/min, IV), respectively. Cardiopulmonary variables were measured at intervals up to 40 min after induction. All horses showed effective sedation following intravenous romifidine or xylazine and achieved recumbency after ketamine administration. There were no significant differences between groups in heart rate, arterial oxygen partial pressures, arterial carbon dioxide partial pressures, cardiac index, stroke index, oxygen delivery, oxygen utilization, systemic vascular resistance, left ventricular work, or any of the measured systemic arterial blood pressures. Cardiac index and left ventricular work fell significantly from baseline while systemic vascular resistance increased from baseline in both groups. The oxygen utilization ratio was higher in the xylazine group at 5 and 15 min after induction. In conclusion, the combination of romifidine/ketamine results in similar cardiopulmonary alterations as a xylazine/ketamine regime, and is a suitable alternative for clinical anesthesia of the horse from a cardiopulmonary viewpoint.     

Cardiovascular effects of a high dose of romifidine in propofol-anesthetized cats

OBJECTIVE: To determine the hemodynamic effects of IM administration of romifidine hydrochloride in propofol-anesthetized cats. ANIMALS: 15 adult domestic shorthair cats. PROCEDURE: Cats were randomly assigned to receive romifidine (0, 400, or 2,000 microg/kg, IM). Cats were anesthetized with propofol and mechanically ventilated with oxygen. The right jugular vein, left carotid artery, and right femoral artery and vein were surgically isolated and catheterized. Heart rate; duration of the PR, QRS, and QT intervals; mean pulmonary artery pressure; mean right atrial pressure; systolic, diastolic, and mean arterial pressures; left ventricular systolic pressure; left ventricular end-diastolic pressure; and cardiac output were monitored. Systemic vascular resistance, rate of change of left ventricular pressure, and rate pressure product were calculated. Arterial and venous blood samples were collected anaerobically for determination of pH and blood gas tensions (Po2 and Pco2). RESULTS: Administration of romifidine at 400 and 2,000 microg/kg, IM, decreased heart rate, cardiac output, rate of change of left ventricular pressure, rate pressure product, and pH. Arterial and pulmonary artery pressures, left ventricular pressure, left ventricular end-diastolic pressure, and right atrial pressure increased and then gradually returned to baseline values. Arterial blood gas values did not change, whereas venous Pco2 increased and venous Po2 decreased. Significant differences between low and high dosages were rare, suggesting that the dosages investigated produced maximal hemodynamic effects. CONCLUSIONS AND CLINICAL RELEVANCE: Romifidine produces cardiovascular effects that are similar to those of other alpha2-agonists. High dosages of romifidine should be used with caution in cats with cardiovascular compromise.     

Cardiopulmonary evaluation of the use of medetomidine hydrochloride in cats.

OBJECTIVE: To evaluate the cardiovascular effects of the alpha2-adrenergic receptor agonist medetomidine hydrochloride in clinically normal cats. ANIMALS: 7 clinically normal cats. PROCEDURE: Cats were anesthetized with isoflurane, and thermodilution catheters were placed for measurement of central venous, pulmonary, and pulmonary capillary wedge pressures and for determination of cardiac output. The dorsal pedal artery was catheterized for measurement of arterial blood pressures and blood gas tensions. Baseline variables were recorded, and medetomidine (20 microg/kg of body weight, IM) was administered. Hemodynamic measurements were repeated 15 and 30 minutes after medetomidine administration. RESULTS: Heart rate, cardiac index, stroke index, rate-pressure product, and right and left ventricular stroke work index significantly decreased from baseline after medetomidine administration, whereas systemic vascular resistance and central venous pressure increased. However, systolic, mean, and diastolic arterial pressures as well as arterial pH, and oxygen and carbon dioxide tensions were not significantly different from baseline values. CONCLUSIONS AND CLINICAL RELEVANCE: When administered alone to clinically normal cats, medetomidine (20 microg/kg, IM) induced a significant decrease in cardiac output, stroke volume, and heart rate. Arterial blood pressures did not increase, which may reflect a predominant central alpha2-adrenergic effect over peripheral vascular effects.     

Comparative cardiovascular, analgesic, and sedative effects of medetomidine, medetomidine-hydromorphone, and medetomidine-butorphanol in dogs

OBJECTIVE: To compare sedative, analgesic, and cardiopulmonary effects after IV administration of medetomidine (20 microg/kg), medetomidine-hydromorphone (20 microg of medetomidine/kg and 0.1 mg of hydromorphone/kg), and medetomidine-butorphanol (20 microg of medetomidine/kg and 0.2 mg of butorphanol tartrate/kg) in dogs. ANIMALS: 6 dogs healthy mixed-breed dogs. PROCEDURE: Instruments were surgically inserted, and heart rate (HR), respiratory rate (RR), systolic arterial pressure (SAP), mean arterial pressure (MAP), diastolic arterial pressure (DAP), mean pulmonary arterial pressure (MPAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), core body temperature, and cardiac output (CO) were measured 0, 5, 10, 15, 30, 45, and 60 minutes after injection. Cardiac index (CI), stroke volume (SV), stroke index (SI), systemic vascular resistance (SVR), and pulmonary vascular resistance (PVR) were calculated. Arterial samples for blood gas analysis were collected 0, 15, and 45 minutes after injection. Intensity of analgesia, degree of sedation, and degree of muscle relaxation were evaluated at aforementioned time points and 75, 90, 120, 150, 180, and 210 minutes after injection. RESULTS: Administration of medetomidine, medetomidine-hydromorphone, and medetomidine-butorphanol was associated with increases in SAP, MAP, DAP, MPAP, PCWP, CVP, SVR, PVR, core body temperature, and PaCO2 and decreases in HR, CO, CI, SV, SI, RR, pH, and PaO2. Clinically important differences were not detected among treatments. Medetomidine-hydromorphone and medetomidine-butorphanol provided a longer duration of sedation and better quality of analgesia, compared with medetomidine alone. CONCLUSIONS AND CLINICAL RELEVANCE: Medetomidine-hydromorphone or medetomidine-butorphanol is associated with improved analgesia and sedation but has cardiopulmonary effects comparable to those for medetomidine alone.     

Effects of acepromazine on the cardiovascular actions of dopamine in anesthetized dogs

OBJECTIVE: To evaluate the effects of acepromazine maleate on the cardiovascular changes induced by dopamine in isoflurane-anesthetized dogs. STUDY DESIGN: Prospective, randomized cross-over experimental design. ANIMALS: Six healthy adult spayed female dogs weighing 16.4 +/- 3.5 kg (mean +/- SD). METHODS: Each dog received two treatments, at least 1 week apart. Acepromazine (0.03 mg kg(-1), IV) was administered 15 minutes before anesthesia was induced with propofol (7 mg kg(-1), IV) and maintained with isoflurane (1.8% end-tidal). Acepromazine was not administered in the control treatment. Baseline cardiopulmonary parameters were measured 90 minutes after induction. Thereafter, dopamine was administered intravenously at 5, 10, and 15 microg kg(-1) minute(-1), with each infusion rate lasting 30 minutes. Cardiopulmonary data were obtained at the end of each infusion rate. RESULTS: Dopamine induced dose-related increases in cardiac index (CI), stroke index, arterial blood pressure, mean pulmonary arterial pressure, oxygen delivery index (DO(2)I) and oxygen consumption index. In the control treatment, systemic vascular resistance index (SVRI) decreased during administration of 5 and 10 microg kg(-1) minute(-1) of dopamine and returned to baseline with the highest dose (15 microg kg (-1) minute(-1)). After acepromazine treatment, SVRI decreased from baseline during dopamine administration, regardless of the infusion rate, and this resulted in a smaller increase in blood pressure at 15 microg kg (-1) minute(-1). During dopamine infusion hemoglobin concentrations were lower following acepromazine and this contributed to significantly lower arterial O(2) content. CONCLUSIONS: Acepromazine prevented the return in SVRI to baseline and reduced the magnitude of the increase in arterial pressure induced by higher doses of dopamine. However, reduced SRVI associated with lower doses of dopamine and the ability of dopamine to increase CI and DO(2)I were not modified by acepromazine premedication. CLINICAL RELEVANCE: Previous acepromazine administration reduces the efficacy of dopamine as a vasopressor agent in isoflurane anesthetized dogs. Other beneficial effects of dopamine such as increased CO are not modified by acepromazine.     

Romifidine and low doses of tiletamine‐zolazepam in dogs

ObjectiveTo evaluate clinical effects of romifidine and low doses of tiletamine‐zolazepam (TZ) in dogs.Study designRandomized “blinded” cross‐over study.AnimalsSix healthy beagle dogs (two males, four females).MethodsIn separate preliminary experiments dogs received intravenous (IV) tiletamine‐zolazepam (TZ) at 1 and 2 mg kg^?1. For the main trial, dogs received romifidine (R) followed 5 minutes later by IV at six dose regimens: R40TZ1, R60TZ1, R80TZ1 (Romifidine at 40, 60, 80 μg kg^?1 and TZ at 1 mg kg^?1), R40TZ2, R60TZ2 and R80TZ2 (Romifidine at 40, 60, 80 μg kg^?1 and TZ at 2 mg kg^?1). Dogs underwent endotracheal intubation, but breathed room air. Cardiorespiratory variables were measured and arterial blood analyzed. Quality of sedation, duration of anaesthesia and time to recovery (TR) were recorded. Data were analysed by anova or Friedman test as relevant.ResultsEndotracheal intubation was possible with all romifidine/TZ combinations but not with TZ alone. Mean times (minutes) from TZ injection to return of pedal reflex were 1–3 minutes for TZ alone, and 9–17 minutes for romifidine combinations. In the main trial (romifidine combinations) mean time (minutes) to standing increased with increasing dosage (R40TZ1 13; R80TZ2 32). Five minutes after TZ administration, when compared with baseline arterial blood pressures and arterial carbon dioxide had increased, and respiratory rate, pH and arterial oxygen tensions decreased, these changes becoming statistically significant with the higher dose rates. One dog in R60TZ2 and three dogs in R80TZ2 became hypoxaemic.Conclusions and clinical relevanceRomifidine improves the quality and lengthens the duration of anaesthesia induced by TZ. The combination provides a suitable protocol for induction of or short‐term anaesthesia in healthy dogs. However, the higher doses cause cardiovascular stimulation and respiratory depression, and precautions should be taken accordingly.     

Cardiovascular effects of romifidine in the standing horse

The cardiovascular effects of romifidine, an alpha-2 adrenoreceptor agonist, were investigated in six horses using two doses (80 and 120 microg kg(-1)) in a cross-over study design. Cardiac index and mixed venous oxygenation were significantly decreased at 15 and 30 minutes after both doses of romifidine. Systemic vascular resistance was significantly increased with romifidine (120 microg kg(-1)). Arterial blood pressure increased initially and then gradually decreased; the doses of decrease was significant at 90 and 120 minutes with romifidine 80 and 120 microg kg(-1). There were minimal differences between the two doses of romifidine, and both should be used with care especially in horses with cardiovascular compromise, or when used in combination with other cardiovascular depressant drugs.     

Sedative effects of intramuscular administration of a low dose of romifidine in dogs

OBJECTIVE: To evaluate sedative effects of IM administration of a low dose of romifidine in dogs. ANIMALS: 13 healthy adult Beagles. PROCEDURE: Physiologic saline solution (0.2 ml), 0.1 % romifidine (10, 20, or 40 microg/kg), or 10% xylazine (1 mg/kg) was given IM in a crossover study design. Heart rate, respiratory rate, rectal temperature, hemoglobin saturation, and scores for sedation, muscle relaxation, posture, auditory response, and positioning response were recorded before and at regular intervals for up to 240 minutes after drug administration. RESULTS: Scores for sedation, muscle relaxation, posture, auditory response, and positioning response increased in a dose-dependent manner after romifidine administration. Sedation induced by the highest dose of romifidine (40 microg/kg) was comparable to that induced by xylazine (1 mg/kg). Heart rate, respiratory rate, and rectal temperature decreased in a dose-dependent manner after romifidine administration, but hemoglobin saturation did not change. CONCLUSIONS AND CLINICAL IMPLICATIONS: Romifidine (10, 20, or 40 microg/kg, IM) is an effective sedative in dogs, but causes a decrease in heart rate, respiratory rate, and rectal temperature.     

Sedative and cardiovascular effects of romifidine, alone and in combination with butorphanol, in the horse

The behavioural and sedative effects of intravenous (iv) romifidine (40 and 80 μg/kg bodyweight [bwt]) alone or in combination with iv butorphanol (50 μg/kg bwt) were investigated in four ponies and one Thoroughbred horse. Apparent sedation, as judged by the lowering of the head, and by the response to imposed touch, visual and sound stimuli was assessed. The combination with butorphanol reduced the animals' response to imposed stimuli when compared with the effect of the same dose of romifidine alone. Following the administration of romifidine/butorphanol combinations muzzle tremor was noted and some animals attempted to walk forward. In a separate series, the cardiopulmonary effects of iv romifidine (80 μg/kg bwt) alone, or in combination with butorphanol (50 μg/kg bwt) were investigated. Romifidine and the romifidine/butorphanol combination caused similar cardiovascular changes, these being bradycardia with heart block, and hypertension followed by hypotension. Romifidine caused a transient decrease in arterial oxygen tensions and arterial carbon dioxide tensions had increased significantly by the end of the 90 min recording period. Romifidine/butorphanol combinations produced significantly higher arterial carbon dioxide tensions during the first 15 mins after drug administration than did romifidine alone. Butorphanol at 50 μg/kg bwt iv reduced the response to imposed stimuli in horses sedated with romifidine. The combination produced no cardiovascular changes beyond those induced by romifidine alone, but did increase the degree of respiratory depression.     

Cardiovascular and respiratory effects of ketamine infusions in isoflurane-anesthetized dogs before and during noxious stimulation

OBJECTIVE: To characterize the effects of ketamine administration on the cardiovascular and respiratory systems and on acid-base balance and to record adverse effects of ketamine in isoflurane-anesthetized dogs. ANIMALS: 6 healthy adult mongrel dogs. PROCEDURE: Dogs were anesthetized with isoflurane (1.25 times the individual minimum alveolar concentration) in oxygen, and ketamine was administered IV to target pseudo-steady-state plasma concentrations of 0, 0.5, 1, 2, 5, 8, and 11 microg/mL. Isoflurane concentration was reduced to an equipotent concentration. Cardiovascular, respiratory, and acid-base variables; body temperature; urine production; and adverse effects were recorded before and during noxious stimulation. Cardiac index, stroke index, rate-pressure product, systemic vascular resistance index, pulmonary vascular resistance index, left ventricular stroke work index, right ventricular stroke work index, arterial oxygen concentration, mixed-venous oxygen concentration, oxygen delivery, oxygen consumption, oxygen extraction ratio, alveolar-arterial oxygen partial pressure gradient, and venous admixture were calculated. Plasma ketamine and norketamine concentrations were measured. RESULTS: Overall, ketamine administration improved ventilation, oxygenation, hemodynamics, and oxygen delivery in isoflurane-anesthetized dogs in a dosedependent manner. With the addition of ketamine, core body temperature was maintained or increased and urine production was maintained at an acceptable amount. However, at the higher plasma ketamine concentrations, adverse effects such as spontaneous movement and profuse salivation were observed. Myoclonus and dysphoria were observed during recovery in most dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Infusion of ketamine appears to be a suitable technique for balanced anesthesia with isoflurane in dogs. Plasma ketamine concentrations between 2 to 3 microg/mL elicited the most benefits with minimal adverse effects.     

Naloxone reversal of oxymorphone effects in dogs

Oxymorphone was administered IV to dogs 4 times at 20-minute intervals (total dosage, 1 mg/kg of body weight, IV) on 2 separate occasions. Minute ventilation, mixed-expired carbon dioxide concentration, arterial and mixed-venous pH and blood gas tensions, arterial, central venous, pulmonary arterial, and pulmonary wedge pressures, and cardiac output were measured. Physiologic dead space, base deficit, oxygen transport, and vascular resistance were calculated before and at 5 minutes after the first dose of oxymorphone (0.4 mg/kg) and at 15 minutes after the first and the 3 subsequent doses of oxymorphone (0.2 mg/kg). During 1 of the 2 experiments in each dog, naloxone was administered 20 minutes after the last dose of oxymorphone; during the alternate experiment, naloxone was not administered. In 5 dogs, naloxone was administered IV in titrated dosages (0.005 mg/kg) at 1-minute intervals until the dogs were able to maintain sternal recumbency, and in the other 5 dogs, naloxone was administered IM as a single dose (0.04 mg/kg). Naloxone (0.01 mg/kg, IV or 0.04 mg/kg, IM) transiently reversed most of the effects of oxymorphone. Within 20 to 40 minutes after IV naloxone administration and within 40 to 70 minutes after IM naloxone administration, most variables returned to the approximate values measured before naloxone administration. The effects of oxymorphone outlasted the effects of naloxone; cardiovascular and pulmonary depression and sedation recurred in all dogs. Four hours and 20 minutes after the last dose of oxymorphone, alertness, responsiveness, and coordination improved in all dogs after IM administration of naloxone. Cardiac arrhythmia, hypertension, or excitement was not observed after naloxone administration.     

Comparison of romifidine and medetomidine pre-medication in propofol-isoflurane anaesthetised dogs

The objective of this paper was to evaluate romifidine as a pre-medicant in dogs prior to propofol-isoflurane anaesthesia, and to compare it with medetomidine. For this, eight healthy dogs were anaesthetised. Each dog received three pre-anaesthetic protocols: R40 (romifidine, 40 microg/kg, IV), R80 (romifidine, 80 microg/kg, IV) or MED (medetomidine, 10 microg/kg, IV). Induction of anaesthesia was delivered with propofol and maintained with isoflurane. The following variables were studied before sedative administration and 10 min after sedative administration: heart rate (HR), mean arterial pressure (MAP), systolic arterial pressure (SAP) and diastolic arterial pressure (DAP) and respiratory rate (RR). During maintenance, the following variables were recorded at 5-min intervals: HR, MAP, SAD, DAP, arterial oxygen saturation (SpO(2)), end-tidal CO(2)(EtCO(2)), end-tidal concentration of isoflurane (EtISO) required for maintenance of anaesthesia and tidal volume (TV). Time to extubation, time to sternal recumbency and time to standing were also registered. HR and RR experimented a significantly decreased during sedation in all protocols respect to baseline values. Mean HR, MAP, SAP, DAP, SpO(2), EtCO(2), and TV during anaesthesia were similar for the three protocols. End tidal of isoflurane concentration was statistically similar for all protocols. Recovery time for R40 was significantly shorter than in R80 and MED. The studied combination of romifidine, propofol and isoflurane appears to be an effective drug combination for inducing and maintaining general anaesthesia in healthy dogs.     

Cardiovascular effects of doxacurium chloride in isoflurane-anaesthetised dogs

The cardiovascular effects of doxacurium were studied in 6 isoflurane-anaesthetised dogs. Each dog was anaesthetised twice, receiving doxacurium (0.008 mg/kg bwt) or placebo iv. Dogs were ventilated to normocapnia. Heart rate, cardiac index, systolic, diastolic, and mean arterial blood pressures, stroke volume, pulmonary vascular resistance, pulmonary artery wedge pressure, systemic vascular resistance, and pulmonary arterial pressure were determined. Neuromuscular blockade was assessed using the train-of-four technique. After recording baseline values, dogs randomly received either doxacurium or placebo iv, and data were recorded at 5, 10, 15, 30, 45, 60, 75, 90, 105 and 120 min. At 120 min, dogs treated with doxacurium received edrophonìum (0.5 mg/kg bwt iv) to antagonise neuromuscular blockade; dogs treated with placebos received saline iv. No statistically significant differences were detected after doxacurium compared to placebo. In both the doxacurium and placebo groups, significant increases in systolic arterial blood pressure, cardiac index, and stroke volume and a significant decrease in systemic vascular resistance occurred with time. Doxacurium depressed twitch tension 100% in all dogs (time to maximal twitch depression, 11 ± 7 min). First twitch tension was less than 10% of baseline values in all dogs at the time (120 min) of edrophonium administration. Additional edrophonium (1.0 ± 0.4 mg/kg iv) was required to obtain a fourth twitch to first twitch ratio of greater than 0.70. In conclusion, doxacurium is a long-acting neuromuscular blocking agent with no significant cardiovascular effects in isoflurane-anesthetised dogs. In dogs, doxacurium is indicated primarily for long surgical procedures requiring neuromuscular blockade and cardiovascular stability.     

Cardiovascular effects of propofol alone and in combination with ketamine for total intravenous anesthesia in cats

OBJECTIVE: To compare cardiovascular effects of equipotent infusion doses of propofol alone and in combination with ketamine administered with and without noxious stimulation in cats. ANIMALS: 6 cats. PROCEDURE: Cats were anesthetized with propofol (loading dose, 6.6 mg/kg; constant rate infusion [CRI], 0.22 mg/kg/min) and instrumented for blood collection and measurement of blood pressures and cardiac output. Cats were maintained at this CRI for a further 60 minutes, and blood samples and measurements were taken. A noxious stimulus was applied for 5 minutes, and blood samples and measurements were obtained. Propofol concentration was decreased to 0.14 mg/kg/min, and ketamine (loading dose, 2 mg/kg; CRI, 23 microg/kg/min) was administered. After a further 60 minutes, blood samples and measurements were taken. A second 5-minute noxious stimulus was applied, and blood samples and measurements were obtained. RESULTS: Mean arterial pressure, central venous pressure, pulmonary arterial occlusion pressure, stroke index, cardiac index, systemic vascular resistance index, pulmonary vascular resistance index, oxygen delivery index, oxygen consumption index, oxygen utilization ratio, partial pressure of oxygen in mixed venous blood, pH of arterial blood, PaCO2, arterial bicarbonate concentration, and base deficit values collected during propofol were not changed by the addition of ketamine and reduction of propofol. Compared with propofol, ketamine and reduction of propofol significantly increased mean pulmonary arterial pressure and venous admixture and significantly decreased PaO2. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of propofol by CRI for maintenance of anesthesia induced stable hemodynamics and could prove to be clinically useful in cats.     

Sedative, analgesic and cardiorespiratory effects of romifidine in cats

OBJECTIVE: To evaluate the sedative, analgesic, and cardiorespiratory effects of intramascular (IM) romifidine in cats. STUDY DESIGN: Prospective, randomized experimental trial. ANIMALS: Ten healthy adult cats. METHODS: Romifidine (100, 200, and 400 microg kg(-1)) or xylazine (1 mg kg(-1)) was given IM in a cross-over study design. Heart rate (HR), respiratory rate (RR), rectal temperature (RT), hemoglobin saturation, oscillometric arterial pressure, and scores for sedation, muscle relaxation, position, auditory response, and analgesia were determined before and after drug administration. Time to recumbency, duration of recumbency, and time to recover from sedation were determined. Subjective evaluation and cardiorespiratory variables were recorded before and at regular intervals for 60 minutes after drug administration. RESULTS: Bradycardia developed in all cats that were given romifidine or xylazine. No other significant differences in physiologic parameters were observed from baseline values or between treatments. Increasing the dose of romifidine did not result in increased sedation or muscle relaxation. Cats given xylazine showed higher sedation and muscle relaxation scores over time. Analgesia scores were significantly higher after administration of romifidine (400 microg kg(-1)) and xylazine (1 mg kg(-1)) than after romifidine at 100 or 200 microg kg(-1). Duration of lateral recumbency was not significantly different between treatments; however, cats took longer to recover after administration of 400 micro g kg(-1) romifidine. CONCLUSIONS AND CLINICAL RELEVANCE: Bradycardia is the most important adverse effect after IM administration of romifidine at doses ranging from 100 to 400 microg kg(-1) or 1 mg kg(-1) of xylazine in cats. The sedative effects of romifidine at 200 microg kg(-1) are comparable to those of 1 mg kg(-1) of xylazine, although muscle relaxation and analgesia were significantly less with romifidine than with xylazine.     

Investigation of romifidine and detomidine for the clinical sedation of horses

The effects of two intravenous doses of romifidine (80 and 120 microg/kg) and one dose of detomidine (20 microg/kg) were compared in a blinded study in 30 horses requiring to be sedated for routine dental treatment. Several physiological parameters were assessed before and for two hours after the administration of the drugs, and the horses' teeth were rasped 30 minutes after they were administered. Romifidine produced a dose-dependent effect on most parameters. Detomidine at 20 microg/kg was similar to romifidine at 120 microg/kg in the magnitude of its sedative effects, but was similar to romifidine at 80 pg/kg in its duration. There were no significant differences between the three treatments in terms of the clinical procedure score.