Andrea Fuller

Thermoregulation in pronghorn antelope (Antilocapra americana Ord) in the summer.

SUMMARY We have used thermistor/data logger assemblies to measure temperatures in the brain, carotid artery, jugular vein and abdominal cavity, and subcutaneously, in five pronghorn antelope over a summer in Wyoming. Globe and air temperature varied by up to ∼50°C daily during the summer and maximum solar radiation was ∼900 W m–2. Brain temperature (38.9±0.3°C) was consistently ∼0.2–0.5°C higher than carotid blood temperature (38.6±0.3°C), which was the same as abdominal temperature (38.8±0.4°C). Jugular blood temperature (38.0±0.4°C) varied, probably because of changes in Respiratory Evaporative Heat Loss (REHL), and was lower than other temperatures. Subcutaneous temperature (38.3±0.6°C) varied, probably because of peripheral vasoactivity, but on average was similar to other temperatures. Carotid blood temperature had a circadian/nycthemeral rhythm weakly but significantly (r=0.634) linked to the time of sunrise, of amplitude 0.8±0.1°C. There were daily variations of up to 2.3°C in carotid body temperature in individual animals. An average range of carotid blood temperature of 3.1±0.4°C over the study period was recorded for the group, which was significantly wider than the average variation in brain temperature (2.3±0.6°C). Minimum carotid temperature (36.4±0.8°C) was significantly lower than minimum brain temperature (37.7±0.5°C), but maximum brain and carotid temperatures were similar. Brain temperature was kept relatively constant by a combination of warming at low carotid temperatures and cooling at high carotid temperatures and so varied less than carotid temperature. This regulation of brain temperature may be the origin of the amplitude of the average variation in carotid temperature found, and may confer a survival advantage.

Thermoregulation in pronghorn antelope (Antilocapra americana,Ord) in winter

SUMMARY Conservation of energy is a prerequisite thermoregulatory strategy for survival in northern hemisphere winters. We have used thermistor/data logger assemblies to measure temperatures in the brain, carotid artery, jugular vein and abdominal cavity, in pronghorn antelope to determine their winter body temperature and to investigate whether the carotid rete has a survival role. Over the study period mean black globe and air temperature were– 0.5±3.2°C and –2.0±3.4°C, respectively, and mean daytime solar radiation was ∼186 W m–2. Brain temperature (Tbrain, 39.3±0.3°C) was higher than carotid blood temperature (Tcarotid, 38.5±0.4°C), and higher than jugular temperature (Tjugular, 37.9±0.7°C). Minimum Tbrain (38.5±0.4°C) and Tcarotid (37.8±0.2°C) in winter were higher than the minimum Tbrain (37.7±0.5°C) and Tcarotid (36.4±0.8°C) in summer that we have reported previously. Compared with summer, winter body temperature patterns were characterized by an absence of selective brain cooling (SBC), a higher range of Tbrain, a range of Tcarotid that was significantly narrower (1.8°C) than in summer (3.1°C), and changes in Tcarotid and Tbrain that were more highly correlated (r=0.99 in winter vs r=0.83 in summer). These findings suggest that in winter the effects of the carotid rete are reduced, which eliminates SBC and prevents independent regulation of Tbrain, thus coupling Tbrain to Tcarotid. The net effect is that Tcarotid varies little. A possible consequence is depression of metabolism, with the survival advantage of conservation of energy. These findings also suggest that the carotid rete has wider thermoregulatory effects than its traditional SBC function.

Hypoxia following etorphine administration in goats (Capra hircus) results more from pulmonary hypertension than from hypoventilation

BackgroundEtorphine, a potent opioid agonist, causes pulmonary hypertension and respiratory depression. Whether etorphine-induced pulmonary hypertension negatively influences pulmonary gas exchange and exacerbates the effects of ventilator depression and the resultant hypoxemia is unknown. To determine if these effects occurred we instrumented twelve goats with peripheral and pulmonary arterial catheters to measure systemic and pulmonary pressures before and after etorphine administration. Concurrent cardiopulmonary and arterial blood gas variables were also measured.ResultsEtorphine induced hypoventilation (55% reduction to 7.6u2009±u20092.7xa0L.min−1, F(11,44)u2009=u200915.2 Pu2009<u20090.0001), hypoxia (<45xa0mmHg, F(11,44)u2009=u20098.6 Pu2009<u20090.0001), hypercapnia (>40xa0mmHg, F(11,44)u2009=u20095.6 Pu2009<u20090.0001) and pulmonary hypertension (mean 23u2009±u20096xa0mmHg, F(11,44)u2009=u20098.2 Pu2009<u20090.0001). Within 6xa0min of etorphine administration hypoxia was twice (F(11,22)u2009=u20093.0 Pu2009<u20090.05) as poor than that expected from etorphine-induced hypoventilation alone. This disparity appeared to result from a decrease in the movement of oxygen (gas exchange) across the alveoli membrane, as revealed by an increase in the P(A-a)O2 gradient (F(11,44)u2009=u20097.9 Pu2009<u20090.0001). The P(A-a)O2 gradient was not correlated with global changes in the ventilation perfusion ratio (Pu2009=u20090.28) but was correlated positively with the mean pulmonary artery pressure (Pu2009=u20090.017, r2u2009=u20090.97), indicating that pulmonary pressure played a significant role in altering pulmonary gas exchange.ConclusionAttempts to alleviate etorphine-induced hypoxia therefore should focus not only on reversing the opioid-induced respiratory depression, but also on improving gas exchange by preventing etorphine-induced pulmonary hypertension.

Nalbuphine and butorphanol reverse opioid-induced respiratory depression but increase arousal in etorphine-immobilized goats (Capra hircus).

OBJECTIVESnTo evaluate and compare the efficacy of two opioid agonist-antagonists, nalbuphine and butorphanol, in reversing etorphine-induced respiratory depression in immobilized goats.nnnSTUDY DESIGNnProspective, crossover, experimental trial conducted at 1753xa0m.a.s.l.nnnANIMALSnEight adult female Boer goats (Capra hircus).nnnMETHODSnEight minutes following immobilization with an intramuscular injection of 0.1xa0mgxa0kg(-1) etorphine, goats were given one of nalbuphine (0.8xa0mgxa0kg(-1) ), butorphanol (0.1xa0mgxa0kg(-1) ) or sterile water intravenously, in random order in three trials. Respiratory rate (fR ), ventilation, tidal volume, oxygen consumption (V˙O2 ) and carbon dioxide production (V˙CO2 ) were measured continuously. Arterial blood samples to determine PaO2 and PaCO2 were taken 2xa0minutes before and at 5xa0minute intervals after etorphine administration for 25xa0minutes.nnnRESULTSnBoth nalbuphine and butorphanol increased mean PaO2 from 44xa0mmHg (5.9xa0kPa) to 63xa0mmHg (8.4xa0kPa) after etorphine administration. Butorphanol, but not nalbuphine, also corrected hypopnea and hypoventilation such that fR increasedxa0from 13xa0±xa04 to 21xa0±xa07xa0breathsxa0minute(-1) (compared with 16xa0±xa06xa0breathsxa0minute(-1) following nalbuphine) and ventilation increased from 4.69xa0±xa03.04 to 6.91xa0±xa04.42xa0Lxa0minute(-1) following butorphanol administration. Despite decreases in PaCO2 following nalbuphine and butorphanol, PaCO2 remained elevated compared with pre-immobilization values [nalbuphine: 34xa0±xa03xa0mmHg (4.5xa0±xa00.3xa0kPa); butorphanol: 34xa0±xa02xa0mmHg (4.5xa0±xa00.3xa0kPa)] throughout the immobilization. Both agents also decreased the level of immobilization, and increased V˙O2 and V˙CO2 .nnnCONCLUSIONSnNalbuphine and butorphanol significantly improved respiratory function in immobilized goats, with butorphanol eliciting a greater positive response than nalbuphine. However, both opioid agonist-antagonists partly reversed etorphine-induced immobilization.nnnCLINICAL RELEVANCEnButorphanol and nalbuphine can be used to improve respiratory parameters in etorphine-immobilized wildlife, with butorphanol being more effective, but unwanted arousal can occur.

Ampakine CX1942 attenuates opioid-induced respiratory depression and corrects the hypoxaemic effects of etorphine in immobilized goats (Capra hircus)

OBJECTIVESnTo determine whether CX1942 reverses respiratory depression in etorphine-immobilized goats, and to compare its effects with those of doxapram hydrochloride.nnnSTUDY DESIGNnA prospective, crossover experimental trial conducted at 1753xa0m.a.s.l.nnnANIMALSnEight adult female Boer goats (Capra hircus) with a meanxa0±xa0standard deviation mass of 27.1xa0±xa01.6xa0kg.nnnMETHODSnFollowing immobilization with 0.1xa0mgxa0kg(-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 PaO2 , PaCO2 , pH and SaO2 were taken 2xa0minutes before and then at 5xa0minute intervals after drug administration for 25xa0minutes.nnnRESULTSnDoxapram corrected etorphine-induced respiratory depression but also led to arousal and hyperventilation at 2xa0minutes after its administration, as indicated by the low PaCO2 (27.8xa0±xa04.5xa0mmHg) and ventilation of 5.32xa0±xa05.24xa0Lxa0minute(-1) above pre-immobilization values. CX1942 improved respiratory parameters and corrected etorphines hypoxaemic effects more gradually than did doxapram, with a more sustained improvement in PaO2 and SaO2 in comparison with the control trial.nnnCONCLUSIONSnCX1942 attenuated opioid-induced respiratory depression and corrected the hypoxaemic effects of etorphine in immobilized goats.nnnCLINICAL RELEVANCEnAmpakines potentially offer advantages over doxapram, a conventional treatment, in reversing etorphine-induced respiratory depression without causing unwanted side effects, particularly arousal, in immobilized animals.

Postinduction butorphanol administration alters oxygen consumption to improve blood gases in etorphine-immobilized white rhinoceros

OBJECTIVEnTo investigate the effects of postinduction butorphanol administration in etorphine-immobilized white rhinoceros on respiration and blood gases.nnnSTUDY DESIGNnRandomized crossover study.nnnANIMALSnA group of six sub-adult male white rhinoceros.nnnMETHODSnEtorphine, or etorphine followed by butorphanol 12xa0minutes after recumbency, was administered intramuscularly [2.5xa0mg etorphine, 25xa0mg butorphanol (1000-1250xa0kg), or 3.0xa0mg etorphine, 30xa0mg butorphanol (1250-1500xa0kg)]. Sampling started at 10xa0minutes after initial recumbency, and was repeated at 5xa0minute intervals for 25xa0minutes. Arterial blood gases, limb muscle tremors, expired minute ventilation and respiratory frequency were measured at each sampling point. Calculated values included alveolar-arterial oxygen gradient [ [Formula: see text] ], expected respiratory minute volume (V˙e), tidal volume (Vt), oxygen consumption ( [Formula: see text] ) and carbon dioxide production ( [Formula: see text] ).nnnRESULTSnEtorphine administration resulted in an initial median (range) hypoxaemia [arterial partial pressure of oxygen 25.0 (23.0-28.0) mmHg], hypercapnia [arterial partial pressure of carbon dioxide 76.2 (67.2-81.2) mmHg], increased [Formula: see text] [41.7 (36.6-45.1) mmHg, [Formula: see text] [11.1 (10.0-12.0) Lxa0minute-1] and muscle tremors. Butorphanol administration was followed by rapid, although moderate, improvements in arterial partial pressure of oxygen [48.5 (42.0-51.0) mmHg] and arterial partial pressure of carbon dioxide [62.8 (57.9-75.2) mmHg]. In rhinoceros administered butorphanol, [Formula: see text] [4.4 (3.6-5.1) Lxa0minute-1] and [Formula: see text] [4.2 (3.8-4.4) Lxa0minute-1] were lower than in those not administered butorphanol. Increased arterial oxygen tension was associated with lower oxygen consumption (p=0.002) which was positively associated with lower muscle tremor scores (p<0.0001).nnnCONCLUSIONS AND CLINICAL RELEVANCEnHypoxaemia 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.

Body water conservation through selective brain cooling by the carotid rete: a physiological feature for surviving climate change?

Abstract Mammals with a carotid rete are capable of reducing brain temperature below that of carotid blood temperature, termed selective brain cooling. In artiodactyls, selective brain cooling conserves body water and may provide them with a selective advantage in conditions of increased temperature and aridity.

A structure-function analysis of the left ventricle.

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/cm3 of tissue at rest and was estimated to increase to ∼0.060 W/cm3 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 O2·s-1·cm-3 of tissue at rest to ∼600 nmol O2·s-1·cm-3 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 O2·s-1·cm-3 of mitochondria at rest and ∼3,600 nmol O2·s-1·cm-3 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.

NO EVIDENCE THAT MAMMALS WITHOUT A CAROTID RETE CAN SELECTIVELY COOL THEIR BRAINS

TO THE EDITOR: Middle cerebral artery blood velocity (MCAVmean) is reduced up to 30% in humans following a passive increase in internal temperature of 1–1.5°C (1). If the diameter of the MCA remains unchanged during heat stress, reductions in MCAVmean are proportional to reductions in cerebral blood flow. In support of selective brain cooling in hyperthermic humans, White et al. (7) suggest that vasodilation of the cerebral vasculature exists, which in turn increases cranial perfusion and maintains the arterial-venous temperature difference. The authors state, “it remains to be explained how MCA velocity, and presumably cranial perfusion, is reduced in hyperthermic humans if mean arterial blood pressure is maintained and MCA caliber remains constant” (4, 7). This argument ignores the potent effects of changes in carbon dioxide partial pressures on cerebral perfusion, with hypercapnia increasing and hypocapnia decreasing cerebral blood flow, respectively (6). During moderate to pronounced passive heat stress, arterial and end-tidal carbon dioxide partial pressures decrease upward to 8 Torr (1, 2). Importantly, an 8-Torr reduction in arterial carbon dioxide partial pressure is estimated to reduce cerebral blood flow by 24% (5) through increases in resistance of the cerebral arterioles “downstream” from the MCA (3). Thus the clear and robust reduction in MCAVmean during passive heat stress is likely due primarily to decreases in carbon dioxide partial pressures causing increases in vascular resistance of cerebral arterioles distal to the MCA.

Scaling of morphology and ultrastructure of hearts among wild African antelope

ABSTRACT The hearts of smaller mammals tend to operate at higher mass-specific mechanical work rates than those of larger mammals. The ultrastructural characteristics of the heart that allow for such variation in work rate are still largely unknown. We have used perfusion-fixation, transmission electron microscopy and stereology to assess the morphology and anatomical aerobic power density of the heart as a function of body mass across six species of wild African antelope differing by approximately 20-fold in body mass. The survival of wild antelope, as prey animals, depends on competent cardiovascular performance. We found that relative heart mass (g kg−1 body mass) decreases with body mass according to a power equation with an exponent of −0.12±0.07 (±95% confidence interval). Likewise, capillary length density (km cm−3 of cardiomyocyte), mitochondrial volume density (fraction of cardiomyocyte) and mitochondrial inner membrane surface density (m2 cm−3 of mitochondria) also decrease with body mass with exponents of −0.17±0.16, −0.06±0.05 and −0.07±0.05, respectively, trends likely to be associated with the greater mass-specific mechanical work rate of the heart in smaller antelope. Finally, we found proportionality between quantitative characteristics of a structure responsible for the delivery of oxygen (total capillary length) and those of a structure that ultimately uses that oxygen (total mitochondrial inner membrane surface area), which provides support for the economic principle of symmorphosis at the cellular level of the oxygen cascade in an aerobic organ. Summary: Wild African antelope show proportionality between capillary and mitochondrial investments of the heart, indicating economy of design at the cellular level of the oxygen cascade in an aerobic organ.