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Stroke, Vol 23, 1111-1116, Copyright © 1992 by American Heart Association

ARTICLES

Impairment of endothelium-dependent relaxation in human basilar artery after subarachnoid hemorrhage

K Hatake, I Wakabayashi, E Kakishita and S Hishida
Department of Legal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.

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 KCl, 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 measurements were comparable between the two groups. CONCLUSIONS: These results suggest that the decreased relaxation responses to thrombin and bradykinin occur at the level of endothelial cells and not smooth muscle cells and that decreased relaxation may be involved in delayed vasospasm after subarachnoid hemorrhage. Although the decreased relaxation was observed within 1 day after subarachnoid hemorrhage, a period in which delayed spasm does not occur, this time difference may be dependent on the severity of bleeding after rupture of an aneurysm.

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