To determine the hemodynamic effects
of IM administration of romifidine hydrochloride in
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
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)
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
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
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)