Sedative and cardiopulmonary effects of medetomidine and reversal with atipamezole in desert tortoises (Gopherus agassizii)

Ten desert tortoises (Gopherus agassizii) were given i.m. injections of 150 mu g/kg of medetomidine. Sedation was achieved in all tortoises by 20 min postinjection and was accompanied by a significant decrease in mean heart a nd respiratory rates, systolic. diastolic, and mean ventricular pressures, and mean ventricular partial pressure of oxygen (PO2). There was no change in mean blood pH, HCO3, Na+, K+, ionized calcium values, and mean ventricul ar partial pressure of carbon dioxide (PCO2). There were statistically sign ificant but clinically insignificant changes in mean base excess and pH-cor rected ionized calcium values. Atipamezole given to five of the tortoises a t 0.75 mg/kg i.m. significantly reversed the sedative effects of the medeto midine, with all tortoises returning to a normal state by 30 min after admi nistration of the reversal agent. In comparison. the other five tortoises g iven an equal volume of physiologic saline in place of atipamezole (control group) remained significantly sedated for the duration of the study. In ad dition, the heart rate and ventricular PO2 returned to baseline, but the re spiratory rate and ventricular blood pressures were not significantly alter ed by the atipamezole as compared with those of the control group. These ca rdiopulmonary and physiologic effects are similar to those seen In some dom estic mammals. Medetomidine can be used to safely induce sedation in desert tortoises. For procedures lasting greater than 120 min, supplemental oxyge n should be provided. Atipamezole will reverse the sedation but not all of the cardiopulmonary effects, thus necessitating continued monitoring after reversal. Future studies should address the anesthetic and cardiopulmonary effects of medetomidine in combination with other agents such as ketamine a nd/or butorphanol.