Dietary Treatment of Atherosclerosis Abolishes Hyperresponsiveness to SerotoninImplications for Vasospasm
作者:
Donald Heistad,
Allyn Mark,
Melvin Marcus,
Donald Piegors,
Mark Armstrong,
期刊:
Circulation Research
(OVID Available online 1987)
卷期:
Volume 61,
issue 3
页码: 346-351
ISSN:0009-7330
年代: 1987
出版商: OVID
关键词: cynomolgus monkeys;peripheral circulation;serotonin
数据来源: OVID
摘要:
Diet-induced atherosclerosis in primates impairs vasodilator responses and greatly potentiates vasoconstrictor responses to serotonin. Serotonin may play an important role in the pathogenesis of vasospasm. In diet-induced regression of atherosclerosis, intimal lesions are reduced, but maximal vasodilator responses do not improve, perhaps because of vascular fibrosis. Our goal was to determine whether dietary treatment of atherosclerosis reverses the augmented vasoconstrictor responses to serotonin and thus might reduce susceptibility to vasospasm. Normal cynomolgus monkeys, atherosclerotic monkeys, and atherosclerotic monkeys that were given a normal (regression) diet for 18 months were studied. Morphometric studies indicated that the regression diet reduced lesions in the iliac and femoral artery since intimal area was reduced by about 50%. In the hind limb perfused at constant flow, residual resistance during maximal vasodilatation produced by infusion of adenosine tended to be greater in atherosclerotic monkeys than in normals and failed to improve in regression monkeys. In contrast, vasoconstrictor responses to serotonin were greatly potentiated in atherosclerotic monkeys and were restored to normal in regression monkeys. Serotonin (20 μg i.a.) decreased hind limb resistance (in mm Hg/ml/min) 0.34 ± 0.06 (mean ± SE) in normal monkeys, increased resistance 0.58 ± 0.17 in atherosclerotic monkeys (p < 0.05 vs. normal), and decreased resistance 0.70 ± 0.15 in regression monkeys (p < 0.05 vs. atherosclerotic). Thus, dietary treatment of atherosclerosis abolishes augmented vasoconstrictor responses to serotonin. It is proposed that treatment of atherosclerosis may be beneficial, even when vasodilator responses fail to improve, by reducing susceptibility to serotonin-induced vasospasm.
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