BackgroundOpioid-induced immobilization is associated with severe respiratory depression in the white rhinoceros. We evaluated the efficacy of butorphanol and oxygen insufflation in alleviating opioid-induced respiratory depression in eight boma-managed rhinoceros.ResultsChemical immobilization with etorphine, azaperone and hyaluronidase, as per standard procedure for the white rhinoceros, caused severe respiratory depression with hypoxaemia (PaO2 = 27 ± 7 mmHg [mean ± SD]), hypercapnia (PaCO2 = 82 ± 6 mmHg) and acidosis (pH =7.26 ± 0.02) in the control trial at 5 min. Compared to pre-intervention values, butorphanol administration (without oxygen) improved the PaO2 (60 ± 3 mmHg, F(3,21) =151.9, p <0.001), PaCO2 (67 ± 4 mmHg, F(3,21) =22.57, p <0.001) and pH (7.31 ± 0.06, F(3,21) =27.60, p <0.001), while oxygen insufflation alone exacerbated the hypercapnia (123 ± 20 mmHg, F(3,21) =50.13, p <0.001) and acidosis (7.12 ± 0.07, F(3,21) =110.6, p <0.001). Surprisingly, butorphanol combined with oxygen fully corrected the opioid-induced hypoxaemia (PaO2 = 155 ± 53 mmHg) and reduced the hypercapnia over the whole immobilization period (p <0.05, areas under the curves) compared to the control trial. However, this intervention (butorphanol + oxygen) did not have any effect on the arterial pH.ConclusionsOxygen insufflation combined with a single intravenous dose of butorphanol improved the immobilization quality of boma-managed white rhinoceros by correcting the opioid-induced hypoxaemia, but did not completely reverse all components of respiratory depression. The efficacy of this intervention in reducing respiratory depression in field-captured animals remains to be determined.
Chemical capture is an essential tool in the management and conservation of white rhinoceros ( Ceratotherium simum ); however, cardiovascular responses in immobilized megaherbivores are poorly understood. Blood pressure and heart rate responses in rhinoceros immobilized with etorphine or etorphine plus azaperone, and the effects of subsequent i.v. butorphanol administration were investigated. Six white rhinoceros were used in a randomized crossover study design with four interventions: 1) etorphine i.m.; 2) etorphine plus azaperone i.m.; 3) etorphine i.m. and butorphanol i.v.; and 4) etorphine plus azaperone i.m., and butorphanol i.v. Etorphine resulted in hypertension and tachycardia in immobilized rhinoceros on initial measurements. Over the 25-min study period, blood pressures and heart rate declined. Heart rates were slower, although the rhinoceros were still tachycardic, and blood pressures lower during the whole study period in animals immobilized with etorphine and azaperone compared with those that received only etorphine. Butorphanol administration resulted in lower arterial blood pressures and heart rates in etorphine-immobilized rhinoceros. In rhinoceros immobilized with etorphine and azaperone, heart rate slowed following administration of butorphanol i.v., although blood pressures remained unchanged. Azaperone reduced hypertension associated with etorphine immobilization, but animals remained tachycardic. Administration of butorphanol to etorphine/azaperone-immoblized rhinoceros lowered heart rate to values approaching normal resting levels without altering blood pressure.
Shifting activity to cooler times of day buffers animals from increased heat and aridity under climate change. Conversely, when resources are limited, some nocturnal species become more diurnal, reducing energetic costs of keeping warm at night. Aardvarks (Orycteropus afer) are nocturnal, obligate ant-and termite-eating mammals which may be threatened directly by increasing heat and aridity, or indirectly by the effects of climate change on their prey. We hypothesised that the minimum 24-h body temperature of aardvarks would decline during energy scarcity, and that aardvarks would extend their active phases to compensate for reduced resource availability, possibly resulting in increased diurnal activity when aardvarks were energetically compromised. To measure their thermoregulatory patterns and foraging activity, we implanted abdominal temperature and activity data loggers into 12 adult aardvarks and observed them for varying durations over 3 years in the Kalahari. Under non-drought conditions, aardvarks tightly controlled their 24-h body temperature rhythm (mean amplitude of the 24-h body temperature rhythm was 1.8 ± 0.3 • C during summer and 2.1 ± 0.1 • C during winter) and usually were nocturnal. During a summer drought, aardvarks relaxed the precision of body temperature regulation (mean 24-h amplitude 2.3 ± 0.4 • C) and those that subsequently died shifted their activity to progressively earlier times of day in the weeks before their deaths. Throughout the subsequent winter, the aardvarks' minimum 24-h body temperatures declined, causing exaggerated heterothermy (4.7 ± 1.3 • C; absolute range 24.7 to 38.8 • C), with one individual's body temperature varying by 11.7 • C within 8 h. When body temperatures were low, aardvarks often emerged from burrows during daytime, and occasionally returned before sunset, resulting in completely diurnal activity. Aardvarks also shortened their active periods by 25% during food scarcity, likely to avoid energetic costs incurred by foraging. Despite their physiological and behavioural
Hypoxaemia and hypercapnia in etorphine-immobilized rhinoceros resulted from an increased [ [Formula: see text] ] and increased [Formula: see text] and [Formula: see text] associated with muscle tremors. Rather than being associated with changes in V˙e, it appears that improved blood gases following butorphanol administration were a consequence of decreased [Formula: see text] associated with reduced muscle tremoring.
Objectives: To determine whether CX1942 reverses respiratory depression in etorphineimmobilized goats, and to compare its effects with those of doxapram hydrochloride. Study design:A prospective, crossover experimental trial conducted at 1753 m.a.s.l. Animals:Eight adult female Boer goats (Capra hircus) with a mean ± standard deviation mass of 27.1 ± 1.6 kg. Methods:Following immobilization with 0.1 mg kg −1 etorphine, goats received one of doxapram, CX1942 or sterile water intravenously, in random order in three trials. Respiratory rate, ventilation and tidal volume were measured continuously. Arterial blood samples for the determination of PaO 2 , PaCO 2 , pH and SaO 2 were taken 2 minutes before and then at 5 minute intervals after drug administration for 25 minutes.Results: Doxapram corrected etorphine-induced respiratory depression but also led to arousal and hyperventilation at 2 minutes after its administration, as indicated by the low PaCO 2 (27.8 ± 4.5 mmHg) and ventilation of 5.32 ± 5.24 L minute −1 above pre-immobilization values. CX1942 improved respiratory parameters and corrected etorphine's hypoxaemic effects more gradually than did doxapram, with a more sustained improvement in PaO 2 and SaO 2 in comparison with the control trial.Conclusions: CX1942 attenuated opioid-induced respiratory depression and corrected the hypoxaemic effects of etorphine in immobilized goats.Clinical relevance: Ampakines potentially offer advantages over doxapram, a conventional treatment, in reversing etorphine-induced respiratory depression without causing unwanted side effects, particularly arousal, in immobilized animals.2
Mammals use endogenously produced heat to maintain a high and relatively constant core body temperature (T b ). How they regulate their T b during reproduction might inform us as to what thermal conditions are necessary for optimal development of offspring. However, few studies have measured T b in free-ranging animals for sufficient periods of time to encounter reproductive events. We measured T b continuously in six free-ranging adult female African lions (Panthera leo) for approximately 1 year. Lions reduced the 24 h amplitude of T b by about 25% during gestation and decreased mean 24 h T b by 1.3 + 0.18C over the course of the gestation, reducing incidences of hyperthermia (T b . 39.58C). The observation of improved homeothermy during reproduction may support the parental care model (PCM) for the evolution of endothermy, which postulates that endothermy arose in birds and mammals as a consequence of more general selection for parental care. According to the PCM, endothermy arose because it enabled parents to better control incubation temperature, leading to rapid growth and development of offspring and thus to fitness benefits for the parents. Whether the precision of T b regulation in pregnant lions, and consequently their reproductive success, will be influenced by changing environmental conditions, particularly hotter and drier periods associated with climate change, remains to be determined.
Opioid-induced immobilisation results in severe respiratory impairment in the white rhinoceros. It has therefore been attempted in the field to reverse this impairment with the use of opioid agonist-antagonists, such as nalorphine, nalbuphine, butorphanol and diprenorphine; however, the efficacy of some of these treatments has yet to be determined. The efficacy of butorphanol, either alone or in combination with diprenorphine both with and without oxygen insufflation, in alleviating opioid-induced respiratory impairment was evaluated. The study was performed in two parts: a boma trial and a field trial. Rhinoceroses were immobilised specifically for the study, according to a strict protocol to minimise confounding variables. A two-way analysis of variance was used to compare the physiological responses of the rhinoceroses to the different treatments and their effects over time. The intravenous administration of butorphanol (at 3.3 mg per mg etorphine) plus diprenorphine (at 0.4 mg per mg etorphine) did not offer any advantage over butorphanol (at 15 mg per mg etorphine) alone with regard to improving PaO2, PaCO2 and respiratory rates in etorphine-immobilised white rhinoceroses. Both butorphanol + diprenorphine + oxygen and butorphanol + oxygen, at the doses used, significantly improved the etorphine-induced hypoxaemia in both boma- and field-immobilised white rhinoceroses. Clinically acceptable oxygenation in field-immobilised white rhinoceroses can be achieved by using either treatment regimen, provided that it is combined with oxygen insufflation.
This study presents a structure-function analysis of the mammalian left ventricle and examines the performance of the cardiac capillary network, mitochondria, and myofibrils at rest and during simulated heavy exercise. Left ventricular external mechanical work rate was calculated from cardiac output and systemic mean arterial blood pressure in resting sheep (Ovis aries; n = 4) and goats (Capra hircus; n = 4) under mild sedation, followed by perfusion-fixation of the left ventricle and quantification of the cardiac capillary-tissue geometry and cardiomyocyte ultrastructure. The investigation was then extended to heavy exercise by increasing cardiac work according to published hemodynamics of sheep and goats performing sustained treadmill exercise. Left ventricular work rate averaged 0.017 W/cm of tissue at rest and was estimated to increase to ∼0.060 W/cm during heavy exercise. According to an oxygen transport model we applied to the left ventricular tissue, we predicted that oxygen consumption increases from 195 nmol O·s·cm of tissue at rest to ∼600 nmol O·s·cm during heavy exercise, which is within 90% of the oxygen demand rate and consistent with work remaining predominantly aerobic. Mitochondria represent 21-22% of cardiomyocyte volume and consume oxygen at a rate of 1,150 nmol O·s·cm of mitochondria at rest and ∼3,600 nmol O·s·cm during heavy exercise, which is within 80% of maximum in vitro rates and consistent with mitochondria operating near their functional limits. Myofibrils represent 65-66% of cardiomyocyte volume, and according to a Laplacian model of the left ventricular chamber, generate peak fiber tensions in the range of 50 to 70 kPa at rest and during heavy exercise, which is less than maximum tension of isolated cardiac tissue (120-140 kPa) and is explained by an apparent reserve capacity for tension development built into the left ventricle.
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