Goldstein D S, Keiser H R
Am Heart J. 1984 May;107(5 Pt 1):974-9. doi: 10.1016/0002-8703(84)90837-8.
To determine whether cholinergic mechanisms contribute to blood pressure responses during arterial baroreflex inhibition and stimulation, we assessed the effects of atropine on pressor and depressor responses during and after release of the Valsalva maneuver, upon administration of intravenous phenylephrine and nitroglycerin, and during neck suction in 12 healthy people. Atropinization augmented the depressor response during the Valsalva maneuver (269%), the pressor response after release of the maneuver (544%), the pressor response to phenylephrine (109%), and the depressor response to nitroglycerin (76%), whereas the depressor response to externally applied neck suction was attenuated or abolished in all subjects. Cardiac output as indicated by impedance cardiography was unchanged during carotid baroreceptor stimulation. The results are best explained by inhibition by atropine of compensatory cholinergic heart rate, vasodilator, and negative inotropic responses.
为了确定胆碱能机制是否在动脉压力反射抑制和刺激过程中对血压反应有影响，我们评估了阿托品对12名健康人在瓦尔萨尔瓦动作（Valsalva maneuver）释放期间及之后、静脉注射去氧肾上腺素和硝酸甘油时以及颈部吸引过程中的升压和降压反应的作用。阿托品化增强了瓦尔萨尔瓦动作期间的降压反应（269%）、动作释放后的升压反应（544%）、对去氧肾上腺素的升压反应（109%）以及对硝酸甘油的降压反应（76%），而在所有受试者中，对外加颈部吸引的降压反应减弱或消失。通过阻抗心动描记法测得的心输出量在颈动脉压力感受器刺激期间没有变化。这些结果最好的解释是阿托品抑制了代偿性胆碱能性心率、血管舒张和负性肌力反应。
