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Shock- and Ischemia-Induced Mechanisms of Impairment of Endothelium-Mediated Vasodilation (4)

The responses to ACh and ADP were significantly depressed (p<0.001) after incubation with TNF. However, the responses to A23187 and NaN02 were not altered by TNF. Thus, non-receptor-mediated endothelium-dependent as well as endothelium-independent dilators elicit normal responses after TNF incubation. This confirms the receptor-mediated aspect of the defect in endothelium-dependent dilation by TNF. These data indicate that TNF induces a defect in the endothelium to agents that release EDRF via receptor-mediated mechanisms. Agents that are direct relaxants or that release EDRF directly (ie, without a receptor-activated step) are not inhibited. These findings suggest that TNF alters the surface receptors on endothelial cells but does not inhibit intrinsic EDRF synthesis or release mechanisms. Similar results have been obtained in isolated cat carotid arteries. In these experiments, incubation of the isolated carotid arteries with TNF for 120 min but not 60 min totally abolished the ACh-induced vasorelaxation. Moreover, this inhibition of vasorelaxation induced by TNF was blocked by cycloheximide (20 ji^ml), an inhibitor of protein synthesis.
Tags: coronary artery endothelial dysfunction hypoxia ischemia