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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.

Free access
in American Journal of Veterinary Research

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 (PCO2 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.

Free access
in American Journal of Veterinary Research

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 (PCO2 , 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.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To determine the hemodynamic consequences of the coadministration of a continuous rate infusion (CRI) of medetomidine with a fentanyl bolus in dogs.

Animals—12 healthy sexually intact male dogs weighing 30.3 ± 4.2 kg (mean ± SD).

Procedure—Dogs received either fentanyl alone (15.0 µg/kg, IV bolus) or the same dose of fentanyl during an 11-hour CRI of medetomidine (1.5 µg/kg/h, IV). Prior to drug administration, dogs were instrumented for measurement of cardiac output, left atrial pressure, and systemic arterial blood pressures. Additionally, blood samples were collected from the pulmonary artery and left atrium for blood gas analysis.

Results—Medetomidine infusion reduced the cardiac index, heart rate, and O2 delivery while increasing left atrial pressure. Subsequent fentanyl administration further decreased the cardiac index. The PaO2 was not significantly different between the 2 treatment groups; however, fentanyl transiently decreased PaO2 from baseline values in dogs receiving a CRI of medetomidine.

Conclusions and Clinical Relevance—Because of the prolonged hemodynamic changes associated with the CRI of medetomidine, its safety should be further evaluated before being clinically implemented in dogs. (Am J Vet Res 2005;66:1222–1226)

Full access
in American Journal of Veterinary Research