Stroke, Vol 17, 1209-1214, Copyright © 1986 by American Heart Association
K Tamaki, M Armstrong and D Heistad
In this study hemodynamic and morphometric consequences of atherosclerosis
were examined in cynomolgus monkeys. We tested the hypothesis that
atherosclerosis augments cerebral vasoconstrictor responses to serotonin.
We studied 8 normal and 8 atherosclerotic monkeys, which were fed an
atherogenic diet for 17 months. Morphometric studies indicated marked
intimal proliferation of extracranial carotid arteries, with only modest
reduction in the vascular lumen, as atherosclerotic lesions were displaced
outward. Cerebral blood flow was measured with microspheres and
microvascular pressure was measured with a micropipette in pial arteries
approximately 350 microns diameter. Intracarotid infusion of serotonin
reduced microvascular pressure, which indicates constriction of large
arteries upstream, but cerebral blood flow did not decrease. Serotonin
produced a 2-fold greater reduction in cerebral microvascular pressure in
atherosclerotic monkeys than in normal monkeys. Intracarotid histamine
increased flow and hypocapnia reduced flow in both normal and
atherosclerotic monkeys, without altering cerebral microvascular pressure.
We conclude: First, atherosclerosis potentiates constrictor responses to
serotonin in large cerebral arteries. Because platelets release serotonin
when they aggregate, augmentation of responses by atherosclerosis may have
implications for cerebral vascular responses during aggregation of
platelets at carotid lesions. Second, despite marked proliferation of
intima, atherosclerotic lesions are displaced outward during a prestenotic
phase of the disease, so that the lumen is relatively well preserved.
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Effects of atherosclerosis on cerebral vessels: hemodynamic and morphometric studies
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