Cooling and response to hydrogen peroxide in human saphenous vein: role of the endothelium.

摘要

Abstract In the present work we studied the responses of human saphenous vein to H(2)O(2) and effects of moderate cooling on these responses with analysis of the role of endothelium. H(2)O(2) (10(-7)-10(-2) m) induced concentration-dependent contraction in the intact human saphenous vein strips at both temperatures. At 28 degrees C, the maximal contraction induced by H(2)O(2) was significantly lower than that at 37 degrees C. Compared with intact strips, the sensitivity and the maximal contraction to H(2)O(2) were significantly enhanced in endothelium-denuded strips at 37 and 28 degrees C. However, pD(2) values and maximal contractions were not significantly different in endothelium-denuded strips at different temperatures. Pretreatment with N(G)-nitro-l-arginine methyl ester (l-NAME) increased significantly the maximal contraction and sensitivity to H(2)O(2) at 37 and 28 degrees C. The contractions increased by l-NAME were restored by the pre-incubation of l-arginine (10(-3) m) at every temperature studied. The contractile responses of intact human saphenous veins to H(2)O(2) were reduced significantly by 10(-5) m indomethacin at both temperatures. Our results suggest that H(2)O(2)-induced contraction of human saphenous vein are mediated by its direct effect on the smooth muscle and by the generation of products of the cyclooxygenase pathway from the endothelium. Signalling pathways of these contractile effects are the same at 37 and 28 degrees C. Under normal temperature conditions, the contraction to H(2)O(2) is possibly modulated by endothelial nitric oxide. Cooling reduces the contraction to H(2)O(2) by increasing release of nitric oxide.