低温性血管收缩的机制及防治措施的研究

目的 探讨低温性血管收缩的机制和防治措施。方法 采用内皮细胞培养，扫描电镜，离体血管舒缩功能实验技术，观察血管低温性收空与内皮细胞释放血管舒缩因子的关系。结果 低温使内皮完整或去内皮血管环均明显收缩，务砭张力随着温度的下降而增高，去内皮后血管低温性收缩减弱。低温组牛主动脉内皮细胞茶件培养液能使离体大鼠颈总动脉环产生明显收缩反应，提示牛主动脉内皮细胞向培养液向释放了血管收缩因子。３７℃复温或血管舒张

EXPERIMENTAL STUDY OF MECHANISM AND MEASURES OF PREVENTION AND TREATMENT OF HYPOTHERMAL VASOCONSTRICTION

OBJECTIVE: To investigate the mechanism and to explore the measures of prevention and treatment of hypothermal vasoconstriction. METHODS: By the techniques of endothelial cell culture and scanning electron microscopy, and vasomotor functional test of isolated vascular vessels, the relation of hypothermal vasoconstriction and the release of endothelium-derived contractile and vasodilative factors were observed. RESULTS: Hypothermia obviously induced vasoconstriction of isolated vascular vessels, whether endothelium was intact or removed, the lower the temperature, the higher the vascular tension. Removal of endothelium could decrease the effect of vasoconstriction by hypothermia. The conditioned medium of bovine aortic endothelial cell could induce significantly vasoconstriction of isolated rat common neck arterial ring in hypothermia. It indicated that the bovine aortic endothelial cells secreted contractile factors into the medium. Reheating to 37 degrees C or vasodilator or reheating plus vasodilator did not obviously influence the hypothermia-induced vasoconstriction within 2 hours. When reheating to 50 degrees C, vascular tension was decreased, but only changed in range of 28% to 42%. CONCLUSION: Hypothermia vasoconstriction is relative to vasoconstrictor factors secreted by endothelium. Reheating to 37 degrees C or vasodilator does not antagonize the constriction of vascular vessels. Reheating to 50 degrees C only partially eliminates the constrict effect of blood vessels, so the prevention of hypothermia vasoconstriction should be emphasized.