Comparison of etorphine-midazolam and etorphine-azaperone for African buffalo (Syncerus caffer) immobilisation

Abstract

Objective To compare physiological and time variables of etorphine-azaperone (EA) to etorphine-midazolam (EM) immobilisation in African buffalo bulls. Study design Randomised crossover study Animal population A group of ten adult buffalo bulls of mean ± standard deviation 49 ± 19 months old and weighing 353 ± 97 kg. Method Each buffalo was administered, by dart, EA and EM once, one week apart. Once recumbent, the buffalo was instrumented, and physiological variables were recorded at 5-minute intervals, starting at 5 minutes until 20 minutes after recumbence. Opioid antagonist (naltrexone 20 mg mg-1 etorphine dose) was administered at 40 minutes. Induction (dart placement to recumbent) and recovery (naltrexone administration to standing) times were recorded. Arterial and jugular venous blood samples were analysed for gases, acid-base status, and electrolytes at 5 and 20 minutes using a portable blood gas analyser. The arterial to end-tidal carbon dioxide gradient and alveolar to arterial partial pressure of oxygen gradient were calculated. Data were compared between combinations using a general linear mixed model and reported as mean (± standard deviation). Significant findings were set to p < 0.05. Results The doses of etorphine, azaperone and midazolam administered were 0.015 ± 0.001, 0.15 ± 0.01 and 0.16 ± 0.02 mg kg-1, respectively. Induction times for buffalo immobilised with EA was 326 ± 304 seconds (5.4 ± 5.1 minutes) and not different to 247 ± 162 seconds (4.1 ± 2.7 minutes) for EM. The overall mean heart rate for the buffalo immobilised with EA was 113 ± 27 beats minute-1, which was significantly faster compared to 79 ± 22 beats minute-1 for EM (p < 0.001). The respiratory rate, when buffalo were immobilised with EA, was 18 ± 4 breaths minute-1 which was significantly slower compared to 23 ± 7 breaths minute-1 for EM (p < 0.001). The overall mean arterial blood pressure for buffalo immobilised with EA was 102 ± 25 mmHg, which was significantly lower compared to 163 ± 18 mmHg for EM (p < 0.001). The overall mean arterial partial pressure of oxygen for buffalo immobilised with EA was 37 ± 12 mmHg which was not different compared to 43 ± 8 mmHg for EM (p = 0.062). The potassium concentrations of both arterial and venous samples of the EM immobilised buffalo were 4.0 ± 0.4 mmol L-1 and within expected reference intervals, but significantly different compared to 3.7 ± 0.3 mmol L-1 for EA immobilised buffalo (p < 0.01). The other measured electrolytes (sodium, chloride, and ionised calcium) were not different between EA and EM buffalo nor between arterial and venous blood samples within a combination. The majority of the buffalo demonstrated a negative arterial to end-tidal carbon dioxide gradient with alveolar to arterial partial pressure of oxygen gradients greater than 20 mmHg in both EA and EM, however, there were no significant differences between drug combinations. Recovery times were 71 ± 27 seconds (1.2 ± 0.5 minutes) for EA and not different to 86 ± 44 seconds (1.4 ± 0.7 minutes) for EM immobilisation. Conclusion and clinical relevance EM produced an equally effective and reliable immobilisation as EA in buffalo bulls. However, systemic arterial hypertension was a concern in EM and both combinations caused clinically relevant hypoxaemia. However, treatment of this hypoxaemia is questioned as no clinical variables indicated that life-threatening interventions were required. We speculate that an early compensatory response to severe hypoxaemia was most likely present. Astute monitoring is advised with both drug combinations, especially if supplemental oxygen is administered.