Detomidine is an alpha-2 agonist used to provide sedation in horses. Its effects may be reversed with tolazoline. The goal of this study was to investigate the effects of this reversal agent on gas exchange. Five healthy adult horses [weight, 500.4 ± 8.3 kg (mean ± SEM); age, ranging from 6 to 10 years], instrumented with a jugular and a carotid catheter, were given in a random order 6 different treatments. The interval allowed between treatments was at least 2 weeks. The 6 treatment groups were; saline, 1 ml IV, followed 20 minutes later by tolazoline 4 mg/kg IV; detomidine, 5, 10, 15 or 20 ug/kg IV, followed 20 minutes later by tolazoline 4 mg/kg IV; and detomidine, 20 ug/kg IV, followed 20 minutes later by saline 20 ml IV. We measured PaO2, PaCO2, pH, heart rate (HR), and respiratory rate (RR) and calculated alveolar- arteriolar difference in O2 (A-a DO2). Variables were measured at baseline, 10 and 20 minutes after the first injection, and 5, 15, 30, 60 and 120 minutes following the second injection. Data were analyzed using two way ANOVA and the Student-Newman-Keuls technique with results considered significant with P < 0.05. Detomidine alone did not alter PaO2. Tolazoline following saline caused a significant decrease in PaO2 5 minutes after its administration. Values fell from 104.7 ± 2.65 to 88.6 ± 2.65 mmHg. Tolazoline after detomidine also caused a significant decrease in PaO2 at 15 and 30 minutes after its administration but no dose related effect of detomidine was detected. This decrease in PaO2 was profound in a limited number of cases (lowest value was 54.5 mm Hg) and associated with significant increases in A-a DO2. The sedative effect of detomidine appeared to be reversed by tolazoline. Tolazoline did not cause a significant change in the PaCO2 or pH. RR did not change. The HR decreased significantly following the administration of detomidine at all doses, this decrease was reversed by tolazoline. In conclusion tolazoline alone or in combination with detomidine causes a transient decrease in PaO2 that is not explained by hypoventilation but is a result of increased A-a DO2.
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