期刊
STROKE
卷 39, 期 7, 页码 1979-1987出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/STROKEAHA.107.510008
关键词
arterial blood pressure; middle cerebral artery blood velocity; sympathetic activity
资金
- NHLBI NIH HHS [R01 HL 045547] Funding Source: Medline
Background and Purpose - The effect of antihypertensive drugs on autonomic neural control of the cerebral circulation remains unclear. This study was designed to compare middle cerebral artery mean blood velocity responses to acute hypotension with and without alpha(1)-adrenoreceptor blockade (9Prazosin) in young, healthy humans. Methods - Acute hypotension was induced nonpharmacologically in 6 healthy subjects (9mean +/- SE; 28 +/- 2 years) by releasing bilateral thigh cuffs after 9 minutes of suprasystolic resting ischemia before and after an oral dose of Prazosin (91 mg/20 kg body weight). Results - Prazosin had no effect on thigh cuff release-induced reductions in mean arterial pressure and middle cerebral artery mean blood velocity. However, Prazosin attenuated the amount of peripheral vasoconstriction through the arterial baroreflex as evidenced by a slower return of mean arterial pressure to baseline (P = 0.03). Immediately after cuff release, cerebral vascular conductance index increased through cerebral autoregulation and returned to resting values as a result of an increased perfusion pressure mediated through arterial baroreflex mechanisms. The rate of regulation, an index of cerebral autoregulation, was attenuated with Prazosin (control versus Prazosin; rate of regulation = 0.204 +/- 0.020 versus 0.006 +/- 0.053/s, P = 0.037). In addition, as mean arterial pressure was returning to resting values, the rate of change in cerebral vascular conductance index was decreased with Prazosin (90.005 +/- 0.006/s) compared with control (90.025 +/- 0.005/s; P = 0.010). Conclusions - These data suggest that during recovery from acute hypotension, decreases in cerebral vascular conductance index were mediated by increases in arterial blood pressure and sympathetically mediated cerebral vasoconstriction.
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