Venous Contractile Function During and After Hypothermic Exposure

Hypothermia has been shown to have pathophysiological consequences on endothelial and smooth muscle cell functions. The impact of rewarming on vessels is unknown. This study examines the contractile functions of two sets of rabbit external jugular veins, the first after equilibration at 37°C and the second after cooling from 37°C to 20°C for one hour and following rewarming to 37°C. The pharmacologic parameters: E(max) (the maximal response expressed as a ratio of the contraction to 60 mM KC1) and the EC₅₀ concentration, (which produces 50% of the maximal response) were calculated. Nonreceptor-mediated contractile responses (KCl) did not significantly change with cooling or on rewarming. The sensitivity to norepinephrine increased, whereas the E(max) decreased significantly on cooling to 20°C; both parameters returned to control levels on rewarming. Both the histamine sensitivity and E(max) were decreased (P<0.05) with cooling. The E(max) for histamine returned to normal on rewarming. In contrast to norepinephrine, the jugular vein sensitivity to histamine did not fully recover to untreated control values on rewarming. The sensitivity to bradykinin increased (P<0.05) with cooling and remained so on rewarming. The E(max) for bradykinin decreased on cooling and dropped further upon rewarming (P<0.05). Thus, cooling produced a mixed pattern of alterations in response to contractile agonists, and rewarming did not result in a uniform restoration of these responses. These observations may have clinical implications for organ transplantation, for hypothermic surgery, and for individuals accidentally exposed to cold environmental conditions.