作者: David W. Ferguson , William J. Berg , Paul J. Roach , Ron M. Oren , Allyn L. Mark
DOI: 10.1016/0002-9149(92)90998-E
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摘要: Baroreflex control of heart rate, vascular resistance and norepinephrine is impaired in patients with failure, but recent animal studies demonstrate preserved baroreflex sympathetic nerve activity this disorder. Studies were therefore performed to compare efferent muscle 10 normal subjects (age mean +/- SEM 21 1 years) 11 moderate severe failure 48 5 years, New York Heart Association class II IV, left ventricular ejection fraction 19 2%, pulmonary capillary wedge pressure 27 2 mm Hg, cardiac index 2.04 0.22 liters/min/m2). activation was produced by intravenous infusion phenylephrine (0.5 2.0 micrograms/kg/min) deactivation nitroprusside (0.4 2.5 micrograms/kg/min). During infusion, comparable increases arterial (89 99 3 p less than 0.01) (90 0.01). The exhibited significantly attenuated (p 0.01 for vs failure) decreases rate (93 90 6 beats/min, = not significant [NS]) compared (67 58 4 tended sympathoinhibitory responses pressor stimulus. More strikingly, demonstrated impairment during nitroprusside-induced baroreceptor deactivation. In subjects, a decrease 80 0.001) right atrial (4 pressures resultant reflex increase (68 81 (326 74 746 147 U/min, (n 10), NS 77 (6 pressures, did alter (91 97 NS) or (936 155 1179 275 NS).(ABSTRACT TRUNCATED AT 400 WORDS)