Stornetta R L, Guyenet P G, McCarty R C
Neuroscience Program, University of Virginia, Charlottesville 22903.
J Auton Nerv Syst. 1987 Aug;20(2):121-7. doi: 10.1016/0165-1838(87)90109-3.
Heart rate and blood pressure were recorded in conscious, freely behaving rats through a catheter in the tail artery during administration of nitroprusside or phenylephrine through a catheter in the jugular vein. The sympathetic and parasympathetic components were distinguished by treating the rats with atenolol or methyl-atropine. Reflex bradycardia induced by all doses of phenylephrine was almost totally blocked blocked following methyl-atropine treatment. Reflex tachycardia induced by small to moderate doses of nitroprusside was attenuated to an equal extent following atropine or atenolol treatment. A similar experimental schedule was followed with a separate group of rats to determine the effects of pentobarbital and urethane anesthesia on the baroreceptor reflex. Both pentobarbital and urethane equally attenuated the tachycardia response to a decrease in blood pressure. However, pentobarbital anesthesia resulted in a greater attenuation of the bradycardia response to an increase in blood pressure than did urethane anesthesia. These data support the conclusion that the parasympathetic nervous system is primarily responsible for baroreceptor reflex-induced bradycardia in conscious rats. The sympathetic and parasympathetic systems contribute equally to control baroreceptor reflex-induced tachycardia except in extreme acute hypotension when the tachycardia is predominantly due to the activation of sympathetic nerves. The findings of the second experiment indicate that pentobarbital and urethane affect sympathetic systems differently.
在通过颈静脉导管给予硝普钠或去氧肾上腺素期间，通过尾动脉导管在清醒、自由活动的大鼠中记录心率和血压。通过用阿替洛尔或甲基阿托品处理大鼠来区分交感神经和副交感神经成分。甲基阿托品处理后，所有剂量的去氧肾上腺素诱导的反射性心动过缓几乎完全被阻断。小至中等剂量的硝普钠诱导的反射性心动过速在阿托品或阿替洛尔处理后同等程度地减弱。对另一组大鼠采用类似的实验方案来确定戊巴比妥和乌拉坦麻醉对压力感受器反射的影响。戊巴比妥和乌拉坦均同等程度地减弱了对血压降低的心动过速反应。然而，与乌拉坦麻醉相比，戊巴比妥麻醉导致对血压升高的心动过缓反应的减弱程度更大。这些数据支持以下结论：在清醒大鼠中，副交感神经系统主要负责压力感受器反射诱导的心动过缓。除了在极端急性低血压时心动过速主要归因于交感神经激活外，交感神经系统和副交感神经系统对控制压力感受器反射诱导的心动过速的贡献相同。第二个实验的结果表明，戊巴比妥和乌拉坦对交感神经系统的影响不同。
