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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 µg/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 µg/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.

Conclusion and Clinical Relevance—Romifidine produces cardiovascular effects that are similar to those of other α2-agonists. High dosages of romifidine should be used with caution in cats with cardiovascular compromise. (Am J Vet Res 2002;63:1241–1246)

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in American Journal of Veterinary Research


Objective—To determine the effects of IV administration of enalaprilat on cardiorespiratory and hematologic variables as well as inhibition of angiotensin converting enzyme (ACE) activity in exercising horses.

Animals—6 adult horses.

Procedure—Horses were trained by running on a treadmill for 5 weeks. Training was continued throughout the study period, and each horse also ran 2 simulated races at 120% of maximum oxygen consumption. Three horses were randomly selected to receive treatment 1 (saline [0.9% NaCl] solution), and the remaining 3 horses received treatment 2 (enalaprilat; 0.5 mg/kg of body weight, IV) before each simulated race. Treatment groups were reversed for the second simulated race. Cardiorespiratory and hematologic data were obtained before, during, and throughout the 1-hour period after each simulated race. Inhibition of ACE activity was determined during and after each race in each horse.

Results—Exercise resulted in significant increases in all hemodynamic variables and respiratory rate. The pH and PO2 of arterial blood decreased during simulated races, whereas PCO2 remained unchanged. Systemic and pulmonary blood pressure measurements and arterial pH, PO2, and PCO2 returned to baseline values by 60 minutes after simulated races. Enalaprilat inhibited ACE activity to < 25% of baseline activity without changing cardiorespiratory or blood gas values, compared with horses administered saline solution.

Conclusions and Clinical Relevance—Enalaprilat administration almost completely inhibited ACE activity in horses without changing the hemodynamic responses to intense exercise and is unlikely to be of value in preventing exercise-induced pulmonary hemorrhage. (Am J Vet Res 2001;62:1008–1013)

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in American Journal of Veterinary Research