Vatner S F, Rutherford J D
J Clin Invest. 1978 Jun;61(6):1593-601. doi: 10.1172/JCI109079.
The effects of carotid chemoreceptor stimulation with intracarotid injections of either nicotine, 0.2 mug/kg, or cyanide, 2 mug/kg, were compared with the effects of bilateral carotid occlusion on left ventricular (LV) pressure, dP/dt, and diameter in conscious dogs instrumented with ultrasonic diameter gauges and miniature pressure gauges. With heart rate maintained constant, carotid chemoreceptor stimulation increased mean arterial pressure by 27+/-3%, LV and diastolic diameter by 4+/-0.9% and LV dP/dt by 21+/-2%. With ventilation controlled during succinylcholine infusion, carotid chemoreceptor stimulation increased mean arterial pressure by 43+/-2% and dP/dt by 37+/-5%, values significantly greater, P < 0.01, than were observed in dogs with spontaneous ventilation. Similarly, in dogs with spontaneous ventilation after vagotomy, carotid chemoreceptor stimulation also increased dP/dt by a greater amount, i.e., by 48+/-9%. The increases in LV end diastolic diameter were not affected significantly by either cholinergic blockade with atropine or beta adrenergic blockade with propranolol. Although cholinergic blockade did not affect the inotropic or pressor responses significantly, beta adrenergic blockade attenuated the pressor response and essentially abolished the inotropic response. Bilateral carotid occlusion increased mean arterial pressure and LV end diastolic diameter by similar amounts to those observed with chemoreceptor stimulation, but increased dP/dt significantly less, P < 0.02, i.e., by 13+/-2%. As was observed with chemoreceptor stimulation, inotropic responses were not affected significantly by cholinergic blockade, but were essentially abolished by beta adrenergic blockade. Thus, in the conscious dog with heart rate constant, carotid chemoreceptor stimulation induces a clear positive inotropic effect, which is greater in the absence of the attenuating influences of pulmonary inflation reflexes, and for an equal elevation in arterial pressure appears to exert a greater increase in myocardial contractility than does carotid baro-receptor unloading.
将尼古丁(0.2微克/千克)或氰化物(2微克/千克)经颈内动脉注射刺激颈动脉化学感受器的效应,与双侧颈动脉结扎对植入超声直径测量仪和微型压力测量仪的清醒犬左心室(LV)压力、dP/dt和直径的效应进行了比较。在心率保持恒定的情况下,刺激颈动脉化学感受器使平均动脉压升高27±3%,左心室和舒张期直径增加4±0.9%,左心室dP/dt增加21±2%。在琥珀酰胆碱输注期间控制通气时,刺激颈动脉化学感受器使平均动脉压升高43±2%,dP/dt升高37±5%,这些值显著更高(P<0.01),高于自主通气犬的观察值。同样,在迷走神经切断术后自主通气的犬中,刺激颈动脉化学感受器也使dP/dt有更大幅度的升高,即升高48±9%。左心室舒张末期直径的增加不受阿托品胆碱能阻断或普萘洛尔β肾上腺素能阻断的显著影响。虽然胆碱能阻断对变力或升压反应没有显著影响,但β肾上腺素能阻断减弱了升压反应并基本消除了变力反应。双侧颈动脉结扎使平均动脉压和左心室舒张末期直径升高的幅度与化学感受器刺激时观察到的相似,但使dP/dt升高显著较少(P<0.02),即升高13±2%。正如化学感受器刺激时所观察到的,变力反应不受胆碱能阻断的显著影响,但基本被β肾上腺素能阻断消除。因此,在心率恒定的清醒犬中,颈动脉化学感受器刺激可诱导明显的正性变力作用,在没有肺膨胀反射减弱影响的情况下作用更强,并且对于相同的动脉压升高,与颈动脉压力感受器卸载相比,似乎对心肌收缩力有更大的增强作用。