The role of alpha1- and beta-adrenoceptors in initiation and development of thermoregulatory reactions during fast and slow cooling.

Ionophoretic application of alpha1- and beta-adrenoceptor blockers into the skin produces no effect on the parameters of thermal homeostasis under thermoneutral conditions. alpha1-Adrenoblocker verapamil inhibits cold shivering during fast and slow cold exposure; it elevates the temperature threshold and moderates the vasoconstrictor response during rapid cooling. These changes are accompanied by a compensatory decrease in the threshold and stimulation of non-shivering thermogenesis. Application of non-selective beta-blocker propranolol had no effect on the temperature thresholds of the thermoregulatory reactions, but augmented the maximum amplitude of shivering during both cooling protocols, thereby compensating the decrease in non-shivering thermogenesis. In the whole organism, block of one type adrenoceptors during cold exposure is accompanied by activation of the compensatory mechanisms mediated by adrenoceptors of the other type.

Effects of slow and rapid cooling on catecholamine concentration in arterial plasma and the skin.

Norepinephrine (NE) and epinephrine (Epi) concentrations in arterial plasma and in skin tissue were measured chromatographically before and after external cooling. Urethan-anesthetized rats were cooled either slowly (0.004-0.006 degrees C/s) or rapidly (0.03- 0.05 degrees C/s). Blood samples were drawn three times from each animal: 1) before cooling and at a rectal temperature decreased 2) by 0.5 degrees C and 3) by 3-4 degrees C. Skin samples were taken from controls and from rapidly or slowly cooled rats at a rectal temperature lowered by 0.5 degrees C. The resting mean values were 36.7 +/- 0.3 degrees C for rectal temperature, 0.62 +/- 0.079 and 1. 09 +/- 0.203 ng/ml for plasma NE and Epi, and 85.6 +/- 4.1 and 137.6 +/- 34.3 ng/g for skin NE and Epi. A decrease in rectal temperature by 0.5 degrees C at rapid cooling produced a 2.6-fold increase of NE and a 2.8-fold increase of Epi in plasma. Concomitantly, there was a significant decrease in skin NE concentration by 28% and Epi by 86%. At a rectal temperature decreased by 0.5 degrees C after slow cooling, plasma catecholamines did not change; at unaltered skin NE concentration, there was a reduction in skin Epi concentration (60%). When rectal temperature was lowered by 3-4 degrees C, the increase in plasma NE was virtually the same at both cooling rates and only plasma Epi increased more after deep rapid cooling than slow cooling. Thus the sympathoadrenal system may be differently activated depending on cooling rate. Rapid cooling, when the dynamic activity of the skin cold receptors is involved in the cold response, may provide conditions for an earlier activation of the sympathoadrenal system. This may evidence the functional significance of the dynamic activity of the skin cold receptors in the formation of the cold defense responses.