Search Results

Abstract

Objective—To evaluate the safety of moxidectin administration at doses of 30, 60, and 90 µg/kg of body weight (10, 20, and 30 times the manufacturer's recommended dose) in avermectin-sensitive Collies.

Animals—24 Collies.

Procedure—Collies with mild to severe reactions to ivermectin challenge (120 mg/kg; 20 times the recommended dose for heartworm prevention) were used. Six replicates of 4 dogs each were formed on the basis of body weight and severity of reaction to ivermectin test dose. Within replicates, each dog was randomly allocated to treatment with oral administration of 30, 60, or 90 µg of moxidectin/kg or was given a comparable volume of placebo tablet formulation. Dogs were observed hourly for the first 8 hours and twice daily thereafter for 1 month for signs of toxicosis.

Results—Signs of toxicosis were not observed in any control group dog throughout the treatment observation period. Likewise, signs of toxicosis were not observed in any dog receiving moxidectin at 30, 60, or 90 µg/kg.

Conclusions and Clinical Relevance—The moxidectin formulation used in the study reported here appears to have a wider margin of safety than ivermectin or milbemycin in avermectin-sensitive Collies. (Am J Vet Res 2000;61:482–483)

Abstract

Objective—To determine the relationship between bispectral index (BIS) and minimum alveolar concentration (MAC) multiples of isoflurane after IM injection of medetomidine or saline (0.9% NaCl) solution in anesthetized dogs.

Animals—6 dogs.

Procedure—Each dog was anesthetized 3 times with isoflurane. First, the MAC of isoflurane for each dog was determined by use of the tail clamp method. Second, anesthetized dogs were randomly assigned to receive an IM injection of medetomidine (8 µg · kg^–1) or an equal volume of isotonic saline (0.9% NaCl) solution 30 minutes prior to beginning BIS measurements. Last, anesthetized dogs received the remaining treatment (medetomidine or isotonic saline solution). Dogs were anesthetized at each of 4 MAC multiples of isoflurane. Ventilation was controlled and atracurium (0.2 mg/kg followed by 6 µg/kg/min as a continuous infusion, IV) administered. After a 20-minute equilibration period at each MAC multiple of isoflurane, BIS data were collected for 5 minutes and median values of BIS calculated.

Results—BIS significantly decreased with increasing MAC multiples of isoflurane over the range of 0.8 to 2.0 MAC. Mean (± SD) MAC of isoflurane was 1.3 ± 0.2%. During isoflurane-saline anesthesia, mean BIS measurements at 0.8, 1.0, 1.5, and 2.0 MAC were 65 ± 8, 60 ± 7, 52 ± 3, and 31 ± 28, respectively. During isoflurane-medetomidine anesthesia, mean BIS measurements at 0.8, 1.0, 1.5, and 2.0 MAC were 77 ± 4, 53 ± 7, 31 ± 24, and 9 ± 20, respectively.

Conclusions and Clinical Relevance—BIS monitoring in dogs anesthetized with isoflurane has a predictive value in regard to degree of CNS depression. During isoflurane anesthesia, our results support a MAC-reducing effect of medetomidine. (Am J Vet Res 2003;64:316–320)

Abstract

Objective—To assess duration of actions of butorphanol, medetomidine, and a butorphanol-medetomidine combination in dogs given subanesthetic doses of isoflurane (ISO).

Animals—6 healthy dogs.

Procedure—Minimum alveolar concentration (MAC) values for ISO were determined. for each dog. Subsequently, 4 treatments were administered to each dog (saline [0.9% NaCl] solution, butorphanol [0.2 mg/kg of body weight], medetomidine [5.0 mg/kg], and a combination of butorphanol [0.2 mg/kg] and medetomidine [5.0 mg/kg]). All treatments were administered IM to dogs concurrent with isoflurane; treatment order was determined, using a randomized crossover design. Treatments were given at 7-day intervals. After mask induction with ISO and instrumentation with a rectal temperature probe, endtidal CO₂ and anesthetic gas concentrations were analyzed. End-tidal ISO concentration was reduced to 90% MAC for each dog. A tail clamp was applied 15 minutes later. After a positive response, 1 of the treatments was administered. Response to application of the tail clamp was assessed at 15-minute intervals until a positive response again was detected.

Results—Duration of nonresponse after administration of saline solution, butorphanol, medetomidine, and butorphanol-medetomidine (mean ± SD) was 0.0 ± 0.0, 1.5 ± 1.5, 2.63 ± 0.49, and 5.58 ± 2.28 hours, respectively. Medetomidine effects were evident significantly longer than those for saline solution, whereas effects for butorphanol-medetomidine were evident significantly longer than for each agent administered alone.

Conclusion and Clinical Relevance—During ISOinduced anesthesia, administration of medetomidine, but not butorphanol, provides longer and more consistent analgesia than does saline solution, and the combination of butorphanol-medetomidine appears superior to the use of medetomidine or butorphanol alone. (Am J Vet Res 2000;61:42–47)

Abstract

Objective—To determine the relationship between bispectral index (BIS) and minimum alveolar concentration (MAC) multiples of sevoflurane in cats.

Animals—8 domestic cats.

Procedure—Each cat was anesthetized twice with sevoflurane. First, the MAC of sevoflurane for each cat was determined by use of the tail clamp method. Second, cats were anesthetized with sevoflurane at each of 5 MAC multiples administered in random order. Ventilation was controlled, and after a 15- minute equilibration period at each MAC multiple of sevoflurane, BIS data were collected for 5 minutes and the median value of BIS calculated.

Results—The mean (± SD) MAC of sevoflurane was 3.3 ± 0.2%. The BIS values at 0.5 MAC could not be recorded as a result of spontaneous movement in all 8 cats. The BIS values at 2.0 MAC were confounded by burst suppression in all 8 cats. Over the range of 0.8 to 1.5 MAC, BIS values decreased significantly with increasing end-tidal sevoflurane concentrations. Mean (± SD) BIS measurements were 30 ± 3, 21 ± 3, and 5 ± 2 at 0.8, 1.0, and 1.5 MAC, respectively.

Conclusions and Clinical Relevance—Values of BIS are inversely and linearly related to end-tidal sevoflurane concentrations in anesthetized cats, and BIS may be a useful predictor of CNS depression in this species. The consistently low BIS values recorded in this study suggest that clinical BIS end points used to titrate anesthetic agents in humans may not be applicable to cats. ( Am J Vet Res 2004;65:93–98)

Summary

Eight dogs (body weight, 12.5 to 21.5 kg) were assigned at random to each of 3 treatment groups (is, ix, im) that were not given glycopyrrolate and to each of 3 groups that were given glycopyrrolate (igs, igx, igm). Dogs were anesthetized with isoflurane (1.95% end-tidal concentration), and ventilation was controlled (P_CO2 , 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered iv and im at a dosage of 11 μg/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, im), or medetomidine (15 μg/kg, im) was administered 10 minutes after baseline ade determination. Redetermination of the ade at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0, 2.5, and 5.0 μg/kg/min. The ade was defined as the total dose of epinephrine that induced at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion, or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline and treatment ade values was performed by use of one-way anova. Mean ± sem baseline ade values for groups is, ix, and im were 1.55 ± 0.23, 161 ± 0.28, and 1.95 ± 0.65 μg/kg, respectively. Differences for groups is, ix, and im were – 0.12 ± 0.05, – O.31 ± 0.40, and – 0.17 ± 0.26, respectively. Differences for groups igs, igx, and igm could not be calculated because arrhythmias satisfying the ade criteria were not observed at the maximal infusion rate of 5.0 μg/kg/min. Differences among groups is, ix, and im were not significant. We conclude that in isoflurane-anesthetized dogs: preanesthetic dosages of xylazine (1.1 mg/kg, im) or medetomidine (15 μg/kg, im) do not enhance arrhythmogenicity, and at these dosages, there is no difference in the arrhythmogenic potential of either α₂-adrenergic receptor agonist.

Summary

Hemodynamic and analgesic effects of medetomidine (15 µg/kg of body weight, im) and etomidate (0.5 mg/kg, iv, loading dose; 50 µg/kg/min. constant infusion) were evaluated in 6 healthy adult Beagles. Instrumentation was performed during isoflurane/oxygen-maintained anesthesia. Before initiation of the study, isoflurane was allowed to reach end-tidal concentration ≤ 0.5%, when baseline measurements were recorded. Medetomidine and atropine (0.044 mg/kg) were given im after recording of baseline values. Ten minutes later, the loading dose of etomidate was given im, and constant infusion was begun and continued for 60 minutes. Oxygen was administered via endotracheal tube throughout the study. Analgesia was evaluated by use of the standard tail clamp technique and a direct-current nerve stimulator.

Sinoatrial and atrial-ventricular blocks occurred in 4 of 6 dogs within 2 minutes after administration of a medetomidine-atropine combination, but disappeared within 8 minutes. Apnea did not occur after administration of the etomidate loading dose. Analgesia was complete and consistent throughout 60 minutes of etomidate infusion. Medetomidine significantly (P < 0.05) increased systemic vascular resistance and decreased cardiac output. Etomidate infusion caused a decrease in respiratory function, but minimal changes in hemodynamic values. Time from termination of etomidate infusion to extubation, sternal recumbency, standing normally, and walking normally were 17.3 ± 9.4, 43.8 ± 14.2, 53.7 ± 11.9, and 61.0 ± 10.9 minutes, respectively. All recoveries were smooth and unremarkable. We concluded that this anesthetic drug combination, at the dosages used, is a safe technique in healthy Beagles.

Summary

Eight dogs (12.5 to 21.5 kg) were assigned at random to each of 3 groups that were not given glycopyrrolate (hs, hx, hm) and to each of 3 groups that were given glycopyrrolate (hgs, hgx, hgm). Dogs were anesthetized with halothane (1.31% end-tidal concentration), and ventilation was controlled (P_CO2 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered iv and im at a dosage of 11 μg/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, im, or medetomidine (15 μg/ kg, im) was administered 10 minutes after baseline arrhythmogenic dose of epinephrine (ade) determination. Redetermination of the ade at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0 and 2.5 μg/kg/min. The ade was defined as the total dose of epinephrine inducing at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline ade and posttreatment ade for groups hs, hx, and hm was performed by use of one-way anova. Mean ± sem baseline ade values for groups hs, hx, and hm were 1.50 ± 0.11, 1.49 ± 0.10, and 1.57 ± 0.22 pg/kg, respectively, and for groups hgs, hgx, and hgm were 3.37 ± 0.61, 3.10 ± 0.75, and 3.04 ± 0.94 pg/kg, respectively. Differences for groups hs, hx, and hm were – 0.02 ± 0.15, – 0.00 ± 0.14, and – 0.21 ± 0.17 μg/kg, respectively, and for groups hgs, hgx, and hgm, were – 0.59 ± 0.26, – 0.41 ± 0.15, and – 0.58 ± 0.20 μg/kg, respectively. Differences among groups hs, hx, and hm, or among groups hgs, hgx, and hgm were not significant. We conclude that without and with cholinergic blockade in halothane-anesthetized dogs: preanesthetic dosages of xylazine (1.1 mg/kg, im) or medetomidine (15 μg/kg, im) do not enhance arrhythmogenicity, and at these dosages, there is no difference in the arrhythmogenic potential of either α₂-adrenoceptor agonist.

Summary

Hemodynamic and analgesic effects of medetomidine (30 μg/kg of body weight, im), atropine (0.044 mg/kg, im), and propofol (2 mg/kg, IV, as a bolus, and 165 μg/kg/min, Iv, for 60 minutes, as an infusion) were evaluated in 6 healthy adult Beagles. Catheters were placed while the dogs were anesthetized with isoflurane in oxygen. Administration of isoflurane was then discontinued, and dogs were allowed to breath oxygen until end-tidal isoflurane concentration was ≤ 0.5%. At this time, baseline measurements were recorded and medetomidine and atropine were administered. Ten minutes later, the bolus of propofol was given and the infusion was begun. Analgesia was evaluated with a tail clamp test and by use of a direct-current nerve stimulator. Sinoatrial and atrioventricular blockade developed in all 6 dogs within 2 minutes of administration of medetomidine and atropine, but disappeared within 10 minutes. Apnea did not develop after administration of propofol. Analgesia was strong and consistent throughout the entire 60-minute period of propofol infusion. Medetomidine significantly (P < 0.05) increased systemic vascular resistance and decreased cardiac output, compared with baseline values. Propofol infusion appeared to alleviate medetomidine induced vasoconstriction. Recovery was smooth and uncomplicated. All dogs were able to walk normally at a mean time (± sem) of 88.2 ± 20.6 minutes after termination of propofol infusion. It was concluded that medetomidine, atropine, and propofol, as given in the present study, is a safe combination of anesthetic drugs for use in healthy Beagles.

Abstract

Objective—To evaluate the cardiovascular effects of the α₂-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 µg/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, ratepressure 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 µg/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 α₂-adrenergic effect over peripheral vascular effects. (Am J Vet Res 2001;62:1745–1762)