Cold exposure increases the secretion of catechol amines and enhances the effect of these hormones on metabolism. Whether the sensitivity of peripheral vessels to epinephrine and norepinephrine is altered by cold exposure has not been reported. Warm- adapted (27° ± 1° C) and cold-adapted (5° ± 1 ° C) rabbits were studied under chloralose and urethane anesthesia. Epinephrine and norepinephrine were infused (3 gamma/kg/min) through an ear vein. Rectal plus ear temperature, EKG, blood flow and venous pressure in the ear were measured. Compliance of veins was calculated from the ?V / ?P at pressures between 20 and 30 mm Hg.
After prolonged cold exposure rabbits responded to catechol amine infusion (adrenaline and noradrenaline) with less change in heart rate during infusion and a more rapid return to control levels following infusion; with less decrease in ear temperature during infusion and a more rapid return to control levels following infusion; less increase in peripheral resistance, and less effect on compliance of the capacitance vessels (veins).
The influence of prior cold exposure on vasoconstriction induced by abrupt cold exposure has been studied in the rabbit ear. Dutch breed rabbits were individually caged outdoors (maximum temperature, 21° C; minimum, -7° C; average, 5. 9° C) and a control group was kept at 27° C over a five month period. Three groups of New Zealand rabbits were divided to be exposed to 27° C, 5° C, and 5° C day and 27° C night temperatures.
Rectal, ear and body surface temperatures, heat loss from the ear, and blood flow in the ear were recorded at 27° C, 23° C and 5° C. In general, at 23°and 27° C there was no difference between the groups of rabbits. After one hour exposure to 5° C, outdoor and 5° C groups had a low blood flow to the ear and had no decline in rectal temperature. Other groups, however, had a decrease in rectal temperature and higher ear blood flow. After 12 to 18 hours exposure to 5° C, rectal temperature. returned to original values in the 27° C animals; blood flow to the ear decreased slightly. Ear blood flow in outdoor and 5° C rabbits increased during this period.
A report is presented which briefly characterizes the heat production of the human and the heat exchange with the environment. The mechanisms whereby the temperature control system operates are presented. These characteristics are schematically shown in fourteen figures.
While there is no doubt that the thyroid gland is necessary for the survival of experimental animals at low environmental temperatures, there is little agreement on the role that the thyroid hormone plays in metabolism during prolonged exposure to cold. Sensitizing tissues to adrenalin and increasing neuromuscular activity have been suggested as possible actions of thyroxin. However, the primary effect of cold may be to increase utilization of thyroid hormone by the peripheral tissues. Thyroxin requirement normally remains high for prolonged periods of cold exposure when tested by turnover methods and by replacement experiments. Recent investigations have suggested that thyroxin is synergistic with adrenalin in chemical regulation of heat production, a process markedly enhanced with continuous cold exposure.
The requirement for thyroxin in chemical regulation of heat production was investigated by testing the response of curarized rats to cold exposure at varying periods after thyroidectomy.