Cardiovascular Response of Domestic Ferrets (Mustela putorius furo) to Medetomidine Addition
American Association of Zoo Veterinarians Conference 2000

James S. Gaynor, DVM, MS, DACVA; Eric Monnet, DVM, PhD, DACVS; Jeffrey Wimsatt, DVM, PhD

Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, USA


Medetomidine has been recommended as an adjunct for field application to anesthetize endangered black-footed ferrets and other exotic species. The purpose of the present study was to assess the cardiovascular effect of medetomidine addition in domestic ferrets under controlled sevoflurane anesthesia.

Before study, eight 6.5-month-old male domestic ferrets were surgically implanted as follows with: a Millar® left ventricular catheter, a thoracic aortic flow probe, an abdominal aortic catheter, a doppler monitor on the tail artery for peripheral blood pressure measurement, and right atrial and coronary sinus catheters for microsphere and cardiac function assessment respectively. Cephalic catheters were placed for fluid administration, and volume replacement was matched for each ferret throughout the study period. During the study, performed in muscle paralyzed animals, intermittent positive pressure ventilation (IPPV 10–12 bpm; peak inspiratory pressure 8–12 cm H2O) was employed to maintain an end-tidal PCO2 of 40 mm Hg, and an expired concentration of 1.25% sevoflurane. After stabilization, 40 µg/kg medetomidine was delivered intravenously. Cardiovascular parameters were measured before (0 min), and 1, 2, 3, 5, 10, 15, 30, 45, and 60 min after medetomidine administration.

In response to medetomidine at 1.25% expired sevoflurane concentration, mean arterial pressure was increased (184–114% for the first 15 min), before decreasing steadily to 65% at 60 min. Heart rate decreased 72–79%, and cardiac output dropped immediately with medetomidine, to approximately 37–43% of the awake value (or 70% of the 1.25% sevoflurane value). This decreased output continued throughout the monitoring period.

Likely sources of this sustained drop in cardiac output included a 75% reduction in heart rate and an increased afterload in response to increased peripheral vasoconstriction. In regard to medetomidine, correction of bradycardia and afterload would be useful adjuncts to improve anesthetic safety when partial or complete reversal with a specific antagonist is not possible.


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Jeffrey Wimsatt, DVM, PhD
Department of Clinical Sciences
College of Veterinary Medicine and Biomedical Sciences
Colorado State University
Fort Collins, CO, USA

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