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心包内注射尼古丁诱发的冠状动脉化学反射有躯体成分。

Coronary chemoreflex evoked by intrapericardial nicotine has a somatic component.

作者信息

Pickar J G

机构信息

Department of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan 66506, USA.

出版信息

Am J Physiol. 1997 Feb;272(2 Pt 2):H827-34. doi: 10.1152/ajpheart.1997.272.2.H827.

DOI:10.1152/ajpheart.1997.272.2.H827
PMID:9124445
Abstract

Stimulation of vagally innervated cardiac or pulmonary receptors reflexly evokes depressor responses called the coronary chemoreflex and pulmonary depressor reflex, respectively. The efferent arm of the pulmonary depressor reflex contains a somatic component wherein monosynaptic and polysynaptic muscle reflexes are attenuated. The purpose of the present investigation was to determine whether the efferent arm of the coronary chemoreflex also attenuates the monosynaptic knee-jerk reflex. Cardiac receptors were stimulated by injection of nicotine and bradykinin into the pericardial sac of 15 chloralose-anesthetized (50 mg/kg) cats. The knee-jerk reflex was elicited by tapping the patellar tendon intermittently. Intrapericardial nicotine attenuated the knee-jerk reflex by -26.2 +/- 6.5%. The attenuation was mediated by the vagus nerves, because vagotomy abolished the nicotine-induced attenuation. Stimulation of cardiac receptors evoked the attenuation, because blockade using intrapericardial procaine abolished the nicotine-induced attenuation. On the other hand, intrapericardial bradykinin augmented the knee-jerk reflex by 17.5 +/- 3.3%. The effect was not mediated by the vagus nerves; vagotomy did not abolish the bradykinin-induced augmentation. Changes in the knee-jerk reflex were not correlated with changes in blood pressure or heart rate evoked by intrapericardial nicotine or bradykinin. These findings demonstrate that reflex somatomotor responses accompany the reflex autonomic responses elicited by cardiac receptors. The somatic component of the vagally mediated coronary chemoreflex could contribute to the fainting reaction associated with exertional syncope of aortic stenosis and vasovagal syncope.

摘要

刺激由迷走神经支配的心脏或肺部感受器会分别反射性地引发称为冠状动脉化学反射和肺减压反射的降压反应。肺减压反射的传出支包含一个躯体成分,其中单突触和多突触肌肉反射会减弱。本研究的目的是确定冠状动脉化学反射的传出支是否也会减弱单突触膝跳反射。通过向15只氯醛糖麻醉(50毫克/千克)猫的心包腔内注射尼古丁和缓激肽来刺激心脏感受器。通过间歇性轻敲髌腱来引发膝跳反射。心包内注射尼古丁使膝跳反射减弱了-26.2±6.5%。这种减弱是由迷走神经介导的,因为迷走神经切断术消除了尼古丁引起的减弱。心脏感受器的刺激引发了这种减弱,因为心包内注射普鲁卡因进行阻断消除了尼古丁引起的减弱。另一方面,心包内注射缓激肽使膝跳反射增强了17.5±3.3%。这种效应不是由迷走神经介导的;迷走神经切断术并未消除缓激肽引起的增强。膝跳反射的变化与心包内注射尼古丁或缓激肽引起的血压或心率变化无关。这些发现表明,反射性躯体运动反应伴随着心脏感受器引发的反射性自主反应。迷走神经介导的冠状动脉化学反射的躯体成分可能导致与主动脉瓣狭窄劳力性晕厥和血管迷走性晕厥相关的晕厥反应。

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