| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1991: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1990: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
1. Morphometric analysis of histologic sections of human basilar artery obtained at autopsy was done to determine whether atherosclerotic basilar arteries enlarge in relation to the degree of stenosis of the lumen and to asses whether such enlargement preserves normal cross-sectional area of the lumen. Measurement was done with undistended arteries and corrected to estimate values during distension. The intimal area and percent stenosis (intimal area/internal elastic lamina area x 100) increased with age. At ヲ35 years, none of the specimens had a percent stenosis of >6.0. The internal elastic lamina area correlated positively with the percent stenosis. Neither the lumen area nor the medial area correlated with increasing percentage of stenosis for values of >6.0percent, which show moderate or severe intimal thickening. These results suggest that in atherosclerotic basilar arteries, artery size increases in relation to the degree of stenosis of the lumen, and that lumen is well preserve
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d due to compensatory enlargement of the artery accompanied by decrease in the medial thickness.
2. Using an isometric tension recording method, the author investigated vascular reactivity in isolated human basilar arteries from subjects who died within 1 day after subarachnoid hemorrhage (SAH group) or from subjects who died from causes other than brain involvement (control group). Contraction response to KC1, norepinephrine and 5-hydroxytryptamine did not differ between SAH and control groups. The relaxation response to thrombin, bradykinin and calcium ionophore A23187, which are endotheliumdependent vasodilators, was less for the SAH group than the control group. However, endothelium-independent response to sodium nitroprusside of the SAH group did not differ from that of the control group. These results suggest that the decreased relaxation response to thrombin and bradykinin occurs at the level of endothelial cells and not smooth muscle cells, and that it may be involved in delayed vasospasm after SAH. Less
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