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Using strips of human basilar arteries mounted in organ chambers to record isometric tension, we investigated vascular reactivity to thrombin and bradykinin. Both agents produced endothelium-dependent relaxation of basilar artery strips precontracted with phenylephrine but had no effect on resting tension in strips with or without endotheUum. The relaxations caused by thrombin were abolished by antithrombin III/heparin, hirudin, and MD805. Thrombin but not bradykinin caused complete tachyphylaxis toward a second exposure. Indomethacin did not inhibit the relaxations induced by thrombin or bradykinin, whereas bromophenacyl bromide and methylene blue did. Aging decreased the relaxation induced by thrombin but did not affect the concentration needed to reach 50% maximal relaxation, nor did it affect the maximal relaxation in response to bradykinin, calcium ionophore A23187, and sodium nitroprusside. Our results suggest that thrombin and bradykinin produce endothelium-dependent relaxations mediated by an endothelium-derived relaxing substance and that the relaxation caused by thrombin is mediated by a proteolytic action on endothelial cells. The decrease in relaxations in response to thrombin with increasing age might be due to a decrease in the number or sensitivity of thrombin receptors on endothelial cells. (Stroke 1990;21:1039-1043) A endothelium-derived relaxing substance, discovered by Furchgott and Zawadski 12 and usually called endothelium-derived relaxing factor (EDRF), mediates endothelium-dependent relaxation in response to a number of vasoactive substances. The relaxation decreases in pathophysiological states, such as hypertension 3 and atherosclerosis, 4 and with increasing age, as found in isolated preparations from dogs 5 and rats. 6 We do not know whether the results in experimental animals are applicable to isolated human arteries since there are few studies on this subject.In isolated human basilar arteries, thrombin and bradykinin have recently been shown to induce endothelium-dependent relaxation. 7 -8 Because both vasodilators are known to be generated during blood coagulation, it is important to consider whether vascular responsiveness to them changes with age. The aim of our study was therefore to

Background and Purpose: The goal of this study was to determine the alterations in vascular reactivity of human basilar artery after subarachnoid hemorrhage.Methods: Human basilar arteries were obtained from subjects who died within 1 day after subarachnoid hemorrhage and control subjects who died from causes other than brain involvement. Basilar artery strips were suspended for isometric tension recording in Krebs-Ringer solution. Morphometric study was also carried out on paraffin-embedded sections stained with van Gieson's elastica stain of preselected sites from the basilar arteries. The intimal and medial area and the intimal index ([intimal area/area circumscribed by internal elastic lamina] x 100) were evaluated.Results: Contractile responses to KC1, norepinephrine, and 5-hydroxytryptamine did not differ between subarachnoid hemorrhage and control groups. The endothelium-dependent relaxation responses to thrombin, bradykinin, and calcium ionophore A23187 were less for the subarachnoid hemorrhage group than for the control group. However, the endothelium-independent response to sodium nitroprusside of the subarachnoid hemorrhage group did not differ from that of the control group. Morphometric

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