Stroke, Vol 25, 122-127, Copyright © 1994 by American Heart Association
N Masawa, Y Yoshida, T Yamada, T Joshita, S Sato and B Mihara
BACKGROUND AND PURPOSE--Medial smooth muscle cell necrosis has been
reported as a lesion that may precede angionecrosis, which is a major cause
of not only hypertensive brain hemorrhage but also lacunar infarct. We
morphometrically studied a loss of smooth muscle cells in the media of
cerebral arteries in relation to clinical risk factors. METHODS--The
lateral striate, ie, perforating arteries and the medullary arteries in the
subcortical white matter of the temporal lobe (100 to 400 microns in
diameter) were histologically investigated in 121 autopsied brains. Medial
area was measured quantitatively, and the number of nuclei of smooth muscle
cells in the area was calculated in 1210 cross-sectional arteries of
histological sections. The influence on the structural (ie, smooth muscle
cell) preservation of the tunica media (ratio of number of smooth muscle
cell nuclei to medial area [N- MA ratio]) of age, blood pressure, serum
lipids, and presence of absence of extracerebral severe atherosclerosis was
investigated. RESULTS--The N-MA ratio decreased slightly with age in both
arteries. A reverse correlation between N-MA ratio and age was seen in
groups both with and without hypertension. The mean N-MA ratio in the
hypertensive group was significantly lower than that of the nonhypertensive
group (P < .001) in all decades of life. The mean N-MA ratio of the
perforating arteries was slightly lower than that of the medullary arteries
in both groups. Severe atherosclerosis of the internal carotid arteries,
even with hypertension, mitigated a decrease of the N-MA ratio, which was
as slight as that in the nonhypertensive group. Serum cholesterol in this
group was higher than in both the conventional hypertensive group (P <
.005) and the nonhypertensive group (P < .001). CONCLUSIONS--Although
both hypertension and age were significant risk factors for medial smooth
muscle cell necrosis, hypertension was relatively more significant. Medial
smooth muscle cells of the perforating arteries in the basal ganglia were
more vulnerable than those of the medullary arteries. Cerebral small
arteries in subjects with severe atherosclerosis of the carotid and major
cerebral arteries (hypertension in eight of nine subjects) may have been
protected from extensive loss of medial smooth muscles presumably because
of both high serum cholesterol and decreased wall tensile stress associated
with reduced blood perfusion due to severe atherosclerotic stenosis.
ARTICLES
Morphometry of structural preservation of tunica media in aged and hypertensive human intracerebral arteries
Department of Pathology, Dokkyo University School of Medicine, Tochigi, Japan.
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