Abstract:
Free-living African lions (Panthera leo) are routinely immobilised for veterinary, research and conservation procedures. Ideally, the drugs used for immobilization of free-living lions should result in rapid induction and immobilization with limited adverse cardiorespiratory effects. They also should be reversible or allow for rapid recovery. The currently favoured immobilizing drug combination is tiletamine-zolazepam-medetomidine, which is effective but results in long recovery times. Despite its widespread use, little is known about how this drug combination alters the physiology of immobilised lions captured in the wild. Reducing morbidity risks in immobilised lions through an increased understanding of immobilization-induced cardiorespiratory changes, as well as through improving recovery times, will contribute to future successes in managing wild felids. Other available drug combinations may be suitable for immobilizing lions and improve morbidity risks and recovery times. Ketamine-medetomidine has successfully been used to immobilise lions, but little data is available on the combination’s cardiorespiratory side-effects. The use of ketamine-butorphanol-medetomidine has never been reported for the immobilization of lions but its use has been reported in smaller wild felid species. I therefore investigated how respiratory and cardiovascular function, and immobilization and recovery quality and time, differed in African lions immobilised with tiletamine-zolazepam-medetomidine, ketamine-medetomidine and ketamine-butorphanol-medetomidine. Thirty-six free-living African lions of both sexes and varying ages were immobilised in the Kruger National Park over a period of three months. All three drug combinations caused minor respiratory and metabolic side-effects in the immobilised lions, and no one combination provided an advantage with regards to respiration. Lions immobilised with all three drug combinations were initially mildly hypoxaemic. The initial hypoxaemia was unlikely a consequence of respiratory depression, as lions exhibited respiratory rates on the higher end of normal, and normal ventilation. I determined that the hypoxaemia occurred because the drug combinations, and possibly the stress induced by the immobilization procedure, hindered alveoli oxygen gas exchange, confirmed by high alveolar-arterial gradients and F-shunts.
