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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral vasoconstrictive capacitance was measured during voluntary hyperventilation hypocapnia in 22 healthly normal volunteers aged 21--65 years by serial 133Xe inhalation estimates of rCBF by the initial slope index method of Risberg (ISI2) in the steady state followed by the hypocapnic state. End-tidal PCO2 was monitored by a capnograph. There was significant linear correlation between reduction of PECO2 and the ISI2 values. Significant reduction of cerebral vasoconstrictive response to hypocapnia was found with normal advancing age which is attributed to (1) minor atherosclerosis or loss of elasticity of cerebral vessels with advancing age, (2) the presence of an ischemic threshold during hyperventilation at which CBF tends to stabilize.
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PMID:Normal human aging and cerebral vasoconstrictive responses to hypocapnia. 51 93

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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PMID:Effects of atherosclerosis on cerebral vessels: hemodynamic and morphometric studies. 381 Jul 23