Journal Articles

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    Efficacy and safety of three different opioid-based immobilisation combinations in blesbok (Damaliscus pygargus phillipsi)
    (Medpharm Publications, 2023) Roug A; Smith C; Raath JP; Meyer LCR; Laubscher LL
    African wildlife species are increasingly being immobilised with combinations of a low dose of potent opioids combined with medetomidine and azaperone. The physiological effects of these combinations in comparison to conventional potent opioid-azaperone combinations have scarcely been evaluated. In this cross-over study conducted on eight captive blesbok, we compared the physiological variables of blesbok immobilised with 2 mg of thiafentanil + 10 mg of azaperone (TA); 0.5 mg thiafentanil + 1.5 mg medetomidine (TM), and 0.5 mg thiafentanil + 1.5. mg medetomidine + 10 mg azaperone (TMA). Thiafentanil's effects were antagonised with naltrexone at 10 mg naltrexone per mg thiafentanil, and the medetomidine effects with atipamezole at 5 mg atipamezole per mg medetomidine. The physiological variables were compared between treatment groups using descriptive statistics and repeated measures ANOVA. The TA combination resulted in the shortest induction and recovery times, higher heart rates, respiratory rates, PaO2, SpO2, and lower MAP and A-a gradients, but with less muscle relaxation. The TM and TMA combinations caused marked bradycardia and hypoxaemia. The hypoxaemia was most severe in animals immobilised with TMA, and four of eight blesbok immobilised had a PaO2 < 35 mmHg at the 10- or 15-minute sampling point. These blesbok were provided supplementary oxygen, which corrected the hypoxaemia. The TA combinations caused the lowest degree of physiological compromise. All three combinations were effective for the immobilisation of blesbok, but as the low-dose thiafentanil and high-dose medetomidine combinations caused marked hypoxaemia, supplementary oxygen is recommended when using these combinations.
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    Effects of three immobilizing drug combinations on ventilation, gas exchange and metabolism in free-living African lions (Panthera leo)
    (Oxford University Press and the Society for Experimental Biology, 2023-08-10) Donaldson AC; Buss PE; Fuller A; Meyer LCR; Cooke SJ
    Free-living lions (12 per group) were immobilized with tiletamine-zolazepam-medetomidine (TZM), ketamine-medetomidine (KM), or ketamine-butorphanol-medetomidine (KBM). During immobilization, respiratory, blood gas and acid-base variables were monitored for 30 minutes. Respiratory rates were within expected ranges and remained constant throughout the immobilizations. Ventilation increased in lions over the immobilization period from 27.2 ± 9.5 to 35.1 ± 25.4 L/min (TZM), 26.1 ± 14.3 to 28.4 ± 18.4 L/min (KM) and 23.2 ± 10.8 to 26.7 ± 14.2 L/min (KBM). Tidal volume increased over the immobilization period from 1800 ± 710 to 2380 ± 1930 mL/breath (TZM), 1580 ± 470 to 1640 ± 500 mL/breath (KM) and 1600 ± 730 to 1820 ± 880 mL/breath (KBM). Carbon dioxide production was initially lower in KBM (0.4 ± 0.2 L/min) than in TZM (0.5 ± 0.2 L/min) lions but increased over time in all groups. Oxygen consumption was 0.6 ± 0.2 L/min (TZM), 0.5 ± 0.2 L/min (KM) and 0.5 ± 0.2 L/min (KBM) and remained constant throughout the immobilization period. Initially the partial pressure of arterial oxygen was lower in KBM (74.0 ± 7.8 mmHg) than in TZM (78.5 ± 4.7 mmHg) lions, but increased to within expected range in all groups over time. The partial pressure of arterial carbon dioxide was higher throughout the immobilizations in KBM (34.5 ± 4.2 mmHg) than in TZM (32.6 ± 2.2 mmHg) and KM (32.6 ± 3.8 mmHg) lions. Alveolar-arterial gradients were initially elevated, but decreased over time for all groups, although in KM lions it remained elevated (26.9 ± 10.4 mmHg) above the expected normal. Overall, all three drug combinations caused minor respiratory and metabolic side-effects in the immobilized lions. However, initially hypoxaemia occurred as the drug combinations, and possibly the stress induced by the immobilization procedure, hinder alveoli oxygen gas exchange.
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    Etorphine induces pathophysiology in immobilized white rhinoceros through sympathomimesis that is attenuated by butorphanol
    (y Oxford University Press and the Society for Experimental Biology, 2025-04-04) Boesch JM; Gleed RD; Buss PE; Tordiffe ASW; Zeiler GE; Miller MA; Viljoen F; Harvey BH; Parry SA; Meyer LCR; Madliger C
    White rhinoceros are a sentinel species for important ecosystems in southern Africa. Their conservation requires active management of their population, which, in turn, requires immobilization of individuals with an ultra-potent opioid such as etorphine. Unfortunately, when immobilized with etorphine, they develop severe hypoxaemia that may contribute to morbidity and mortality. We hypothesized that (i) etorphine causes sympathetic upregulation that is responsible for physiological complications that produce hypoxaemia and (ii) butorphanol, a partial μ opioid agonist, mitigates sympathetic upregulation, thereby improving arterial oxygen content (CaO2) and delivery (DO2). Six subadult male white rhinoceros were administered two treatments in random order: etorphine-saline (ES) and etorphine-butorphanol (EB). After intramuscular etorphine (~2.6 μg kg−1), rhinoceros became recumbent (time 0 min [t0]) and were instrumented. Baseline data were collected at t30, butorphanol (0.026 mg/kg) or 0.9% saline was administered intravenously at t37, and data were collected again at t40 and t50. At baseline, plasma noradrenaline concentration was >40 ng ml−1, approximately twice that of non-immobilized rhinoceros (t test, P < 0.05); cardiac output (Qt, by thermodilution) and metabolic rate (VO2, by spirometry/indirect calorimetry) were greater than predicted allometrically (t test, P < 0.05), and pulmonary hypertension was present. After butorphanol, noradrenaline concentration remained greater than in non-immobilized rhinoceros; in EB, CaO2 was greater, while Qt, DO2, VO2, and pulmonary pressures were less than in ES (linear mixed effect model, all P < 0.05). Increased noradrenaline concentration with increased Qt and hypermetabolism supports etorphine-induced sympathetic upregulation. Butorphanol partly attenuated these effects, increasing CaO2 but reducing Qt and, thus, DO2. Since plasma noradrenaline concentration remained increased after butorphanol administration while Qt, DO2, and VO2 decreased, a pathway independent of plasma noradrenaline concentration might contribute to the cardiopulmonary and hypermetabolic effects of etorphine. Developing treatments to combat this sympathomimesis could reduce capture-related morbidity in white rhinoceros.