Etorphine induces pathophysiology in immobilized white rhinoceros through sympathomimesis that is attenuated by butorphanol
Loading...
Date
2025-04-04
Open Access Location
Journal Title
Journal ISSN
Volume Title
Publisher
y Oxford University Press and the Society for Experimental Biology
Rights
(c) 2025 The Author/s
CC BY 4.0
CC BY 4.0
Abstract
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.
Description
Keywords
Butorphanol, Ceratotherium simum, etorphine, hypoxaemia, noradrenaline, sympathetic
Citation
Boesch JM, Gleed RD, Buss PE, Tordiffe ASW, Zeiler GE, Miller MA, Viljoen F, Harvey BH, Parry SA, Meyer LCR. (2025). Etorphine induces pathophysiology in immobilized white rhinoceros through sympathomimesis that is attenuated by butorphanol. Conservation Physiology. 13. 1.