Stephenson R B, Donald D E
Am J Physiol. 1980 Jun;238(6):H815-22. doi: 10.1152/ajpheart.1980.238.6.H815.
Exposure of the vascularly isolated carotid sinuses of 8 conscious dogs to static pressures between 50 and 240 mmHg caused significantly smaller increases [23 +/- 5(SE) mmHg] than decreases (37 +/- 4 mmHg) in arterial pressure frossure and heart rate and shifted the stimulus-response curve upward. Bilateral cervical vagotomy in conscious dogs caused sustained (3 h) increases in arterial pressure (40 +/- 5 mmHg), significantly larger than after atropinization (7 +/- 2 mmHg). In anesthetized, but not in conscious dogs, high sinus pressure reversed the hypertension caused by vagotomy. After vagotomy, low sinus pressure resulted in arterial pressures greater than 200 -mHg. In conscious dogs the carotid baroreflex can widely vary arterial pressure and heart rate despite buffering by extracarotid baroreceptors with vagal afferents, but cannot fully compensate for the acute loss of the latter. Extracarotid baroreceptors actively participate with carotid baroreceptors in the regulation of arterial pressure and better buffer carotid baroreflex-induced increases than decreases in arterial pressure.
对8只清醒犬的血管分离颈动脉窦施加50至240 mmHg的静态压力,导致动脉压和心率的升高[23±5(标准误)mmHg]明显小于降低幅度(37±4 mmHg),并使刺激-反应曲线向上移动。清醒犬双侧颈迷走神经切断术导致动脉压持续(3小时)升高(40±5 mmHg),明显大于阿托品化后(7±2 mmHg)。在麻醉犬而非清醒犬中,高窦压可逆转迷走神经切断术引起的高血压。迷走神经切断术后,低窦压导致动脉压高于200 mmHg。在清醒犬中,尽管有迷走神经传入的颈外压力感受器进行缓冲,颈动脉压力反射仍可广泛改变动脉压和心率,但不能完全补偿后者的急性丧失。颈外压力感受器与颈动脉压力感受器共同积极参与动脉压调节,且对颈动脉压力反射引起的动脉压升高的缓冲作用优于降低作用。