Heart rates, respiratory exchange, and rectal temperatures of five sheep were measured during 4 h exposure to −30 °C and during a 3-h period at +8 °C in which the sheep fed for 1 h. Propranolol, a beta-adrenergic receptor blocking agent, was infused at 0.25, 0.5, and 1.0 mg/kg in both series of experiments. These doses blocked isoproterenol-induced tachycardia. Exposure of the untreated sheep to −30 °C produced marked increases in both energy expenditure and heart rate. Propranolol infusion at 0.25 and 0.5 mg/kg had no effect on energy expenditure but almost totally abolished cardioacceleration in response to cold. Propranolol at 1.0 mg/kg significantly reduced energy expenditure at −30 °C. Both heart rate and energy expenditure increased markedly in the untreated sheep during feeding. Propranolol at 0.25, 0.5, and 1.0 mg/kg had significantly similar effects on heart rate during feeding, reducing the absolute values attained at only 12%. Cardioacceleration during feeding was, however, reduced by 46% because propranolol infusion increased heart rate in the prefeeding period. Propranolol at 0.5 mg/kg had no effect on energy expenditure during feeding. It was concluded that the sympathetic system, acting through the beta receptors, is of major importance in controlling the metabolic and cardiac responses of sheep to acute cold exposure, but of minor importance in initiating and regulating these responses during feeding.

Heat production and thermal insulation were measured in three groups of sheep, control, outdoor, and indoor, which were exposed to the effects of season, cold climate, and cold temperature respectively. The experiment was for 24 weeks, from November 1967 to April 1968. Sheep in the control, outdoor, and indoor groups gained 16.2, 10.0, and 14.9 kg respectively. Average feed intake in both control and outdoor groups was 2.65 kg hay/100 kg sheep per day. Food intake was highest in the indoor group and was inversely related to ambient air temperature. Resting heat production was constant throughout in the control group but increased with time in the outdoor group. Resting heat production in indoor sheep was related to intensity of prior cold exposure. Wool growth and thermal insulation did not differ significantly between groups. Critical temperature for the outside group fell from −15 °C in week 4 to −35 °C in week 20. After these trials, all sheep were shorn. The heat production of the shorn indoor group at −30 °C was greater, and that of the outdoor group was less than that of the controls. The results suggest that, in sheep, acclimation to cold temperatures induces rapid, brief increases in resting heat production and summit metabolism. Acclimatization to cold climates slowly induces a persistent elevation in resting heat production, but appears to reduce the initial metabolic response to an intense cold stimulus.

No abstract

Experiments were performed to assess the role of catecholamines in cold thermogenesis in warm- and cold-acclimated adult sheep. Urinary excretion of both noradrenaline and adrenaline increased in sheep exposed to cold. Propranolol (1 mg/kg) reduced cold thermogenesis in warm- and cold-acclimated sheep by 8% and 12% respectively. Noradrenaline and adrenaline infusions at 1 μg/kg min for 30 min had no significant effect on the rate of heat production of warm- or cold-acclimated sheep. Phenoxybenzamine (3.0 mg/kg) almost abolished cold thermogenesis in warm-acclimated sheep. Cold-acclimated animals treated with phenoxybenzamine were able to maintain homeothermy during severe cold stress. These findings support previous reports which suggest that catecholamines are involved in metabolic cold acclimation in the sheep, but indicate clearly that they have no direct thermogenic effect in cold-acclimated adults of this species.

SUMMARY1. Effects of the natural stimuli of cold exposure and feeding on heart rate were tested in conscious sheep in which blockade of the cardiac efferent nerves was achieved by administration of propranolol and atropine. Effects of direct nerve stimulation, isoproterenol and angiotensin on heart rate before and after autonomic blockade were studied in acute preparations anaesthetized with pentobarbitone sodium.2. Propranolol reduced the extent of cardioacceleration induced both by exposure to cold and by eating. Heart rate in propranolol treated animals exposed to cold did not exceed about 120 beats/min. During eating, heart rate in propranolol treated animals showed no upper limit and increased on occasions to over 170 beats/min.3. Heart rate in conscious sheep following administration of atropine and propranolol was about 110 beats/min; in anaesthetized sheep following vagal section and propranolol it was usually about 120 beats/min. This was taken as intrinsic heart rate.4. Angiotensin administered to normal anaesthetized sheep usually reduced heart rate. After vagal section and propranolol, angiotensin injection usually, and angiotensin infusion invariably, increased heart rate.5. It was concluded that there exists in sheep a mechanism which during eating elevates heart rate by a means other than through the parasympathetic and sympatho-adrenal systems. It is suggested that this mechanism involves a direct chronotropic effect of angiotensin secreted in association with eating.