How can we better assess the cardiopulmonary function of large free-living mammals? — Promaco Conventions
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How can we better assess the cardiopulmonary function of large free-living mammals? (#710)

Adian S Izwan 1 , Edward P Snelling 2 , Roger S Seymour 3 , Leith C R Meyer 2 4 , Andrea Fuller 2 4 , Anna Haw 2 , Duncan Mitchell 1 2 , Anthony P Farrell 5 6 , Mary-Ann Costello 7 , Margaret Badenhorst 8 , Shane K Maloney 1 2
  1. School of Human Sciences, University of Western Australia, Crawley, Western Australia, Australia
  2. Brain Function Research Group, School of Physiology, University of the Witswatersrand, Johannesburg, South Africa
  3. School of Biological Sciences, University of Adelaide, Adelaide, South Australia, Australia
  4. Department of Paraclincal Sciences, University of Pretoria, Pretoria, South Africa
  5. Department of Zoology, University of British Columbia, Vancouver, British Columbia , Canada
  6. Faculty of Land and Food Systems, University of British Columbia, Vancouver, British Columbia, Canada
  7. Central Animal Service, University of the Witswatersrand, Johannesburg, South Africa
  8. School of Physiology, University of the Witswatersrand, Johannesburg, South Africa

Chemical immobilization is often necessary for the study of undomesticated animals, but can have confounding physiological effects on the data collected. We exposed sheep (Ovis aries; n=5) and goats (Capra hircus; n=4) to an immobilizer (etorphine) then transitioned them onto a deeper sedative (propofol) and reversed the etorphine. The cardiopulmonary effects of these drugs were compared with data under a very mild sedative (midazolam). We hypothesized that propofol would provide better data than if animals remained on etorphine. Etorpine caused tachycardia in the sheep (110±14 to 180±7 beats min-1, P<0.001), which abated under propofol (180±7 to 147±6 beats min-1, P<0.05). Etorphine caused a reduced stroke volume in the sheep (53±4 to 35±6 ml, P<0.05), but not the goats. Overall, cardiac output was unchanged in either species. Hypoventilation was seen in the sheep under etorphine (7±2 to 3±0.3 L min-1, P<0.05) before improving under propofol (3±0.3 to 9±2 L min-1, P<0.05). Ventilation in the goats was unaffected. The goats were hypertensive under propofol (71±3 to 101±6 mmHg, P<0.05) but the sheep was unaffected. The mean pulmonary artery pressure of both species increased under etorphine (14±1 to 19±1 mmHg, P<0.05; 14±1 to 20±2 mmHg, P<0.05 respectively), before decreasing under propofol. Both species were relatively hypoxic and hypercapnic under both drugs compared to midazolam (P<0.05), though to a lesser degree under propofol. Many of the side effects observed in both species under etorphine were ameliorated when etorphine was reversed and the animals held under propofol. The data obtained from animals under propofol more accurately reflects the resting state.

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