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 microg/kg of medetomidine. Sedation was achieved in all tortoises by 20 min postinjection and was accompanied by a significant decrease in mean heart and 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 ventricular partial pressure of carbon dioxide (PCO2). There were statistically significant but clinically insignificant changes in mean base excess and pH-corrected ionized calcium values. Atipamezole given to five of the tortoises at 0.75 mg/kg i.m. significantly reversed the sedative effects of the medetomidine, with all tortoises returning to a normal state by 30 min after administration of the reversal agent. In comparison, the other five tortoises given an equal volume of physiologic saline in place of atipamezole (control group) remained significantly sedated for the duration of the study. In addition, the heart rate and ventricular PO2 returned to baseline, but the respiratory rate and ventricular blood pressures were not significantly altered by the atipamezole as compared with those of the control group. These cardiopulmonary and physiologic effects are similar to those seen in some domestic mammals. Medetomidine can be used to safely induce sedation in desert tortoises. For procedures lasting greater than 120 min, supplemental oxygen 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 and/or butorphanol.
Sleeman
J M
JM
Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins 80523, USA.
Gaynor
J
J
D000136:Acid-Base Equilibrium / Q000187:drug effects; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000818:Animals; D001784:Blood Gas Analysis / Q000662:veterinary; D001794:Blood Pressure / Q000187:drug effects; D004573:Electrolytes / Q000097:blood; D006339:Heart Rate / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D006993:Hypnotics and Sedatives / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D007093:Imidazoles / Q000494:pharmacology*; D020926:Medetomidine / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D010100:Oxygen / Q000097:blood; D012119:Respiration / Q000187:drug effects; D014426:Turtles / Q000502:physiology*
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D004573:Electrolytes; D006993:Hypnotics and Sedatives; D007093:Imidazoles; C050701:atipamezole; D020926:Medetomidine; D010100:Oxygen