Hypothermia has pathophysiological consequences on endothelial and smooth muscle cell function. This study investigates the impact on venous relaxation of hypothermia and rewarming following hypothermic exposure. In vitro isometric relaxation responses of norepinephrine precontracted rabbit external jugular veins to a panel of endothelium-dependent and -independent agonists were assessed in controls at 37°C, and in an experimental group after cooling to 20°C and after rewarming to 37°C. On cooling, the endothelium-dependent responses to acetylcholine became multiphasic with initial contraction at low concentrations followed by relaxation at higher concentrations, the maximum of which was significantly diminished compared to controls. Incubation with indomethacin did not affect this response. Rewarming reestablished a monophasic dose-dependent acetylcholine induced relaxation response but the maximal response was significantly augmented. This augmentation in relaxation on rewarming could be prevented by preincubation with indomethacin. The maximal response to calcium ionophore was reduced at 20°C and augmented upon rewarming to 37°C. All veins relaxed in a dose-dependent manner to the nonendothelium-dependent agonists forskolin and sodium nitroprusside; the maximal responses were significantly reduced at 20°C and returned to normal upon rewarming. This study suggests that short- term exposure of venous tissue to hypothermia impairs the vessel's ability to produce endothelium-dependent relaxation. Rewarming does not re-establish normal endothelium-dependent relaxation but results in an enhanced, partially indomethacin-sensitive, response which appears to be independent of changes in nonendothelium-dependent mediated relaxation.
- endothelial cells
- smooth muscle cells
- vasomotor function
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine