Intracardiac route of the Bezold-Jarisch reflex.

Intracardiac route of the Bezold-Jarisch reflex.
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Bezold-Jarisch 反射的心内路线。

DOI:
10.1152/ajplegacy.1971.221.5.1464
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发表时间:
1971
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
T. James
T. James
中科院分区:
--
文献类型:
--
作者:
R. Frink;T. James

文献摘要

被引文献

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理查德·弗林克,和托马斯N。James.贝-雅二氏反射的心内路径。Am. J. Physiol.221(5):1464-1469. 1971.-贝-雅二氏反射起源于左心室,产生窦性心动过缓和动脉低血压。虽然已知该反射是通过迷走神经介导的,但其心内途径尚不清楚。我们的实验考虑了三种可能的从左心室传入的途径:1)与冠状静脉一起到达冠状窦并从那里流出心脏,2)与浦肯野系统一起到达左室间隔内膜,然后通过希氏束回到冠状窦,3)与冠状动脉一起到达主动脉根部。通过插管远端左回旋动脉,选择性灌注2 y 0利多卡因阻断第一路线;通过插管间隔动脉,选择性灌注利多卡因阻断第二路线;通过动脉周围浸润利多卡因周围的主要左冠状动脉,阻断第三路线。前两种手术均产生房室传导阻滞,但三种手术均未改变正常窦房结对迷走神经刺激(直接或反射)的反应性。26只狗用戊巴比妥钠麻醉,在左前降支动脉内注射尼古丁有规律地诱发反射。在10只狗中,通过直接灌注到远端左旋支动脉的局部麻醉和AV阻滞的产生未能改变反射性窦性心动过缓。在11只狗中,通过直接灌注到隔动脉中来产生麻醉性AV阻滞未能改变反射性窦性心动过缓。在四只狗中,两个部位的利多卡因麻醉仍然未能消除反射。在7只狗的左冠状动脉周围局部浸润利多卡因,阻断了所有7只狗的反射。我们的结论是Bezold-Jaris反射漏斗的心内路径朝向左冠状动脉主干的起源,从心脏流出。实验性房室传导阻滞;反射性窦性心动过缓BEZOLD-JARISCH反射已被发现约100年(2,19,20,24)。其主要心血管成分是心动过缓和动脉低血压。虽然生理学家和药理学家早已熟悉,但它通常被认为是实验室的一个奇怪之处。然而,心动过缓和低血压是人类急性后壁心肌梗死期间常见的临床观察结果,并且这些通常(但不总是)对阿托品的给药有显著反应,这表明它们代表了实验反射的人类对应物(1,10,11,16,28,30)。典型的实验反射是由尼古丁或藜芦碱对左心室受体的化学刺激引起的。尽管有人认为这种反射是由冠状动脉化学感受器介导的(5),但Sleight(29)能够通过左侧局部麻醉消除对局部应用尼古丁的反应
FRINK, RICHARD J., AND THOMAS N. JAMES. Intracardiac route of the Bezold-Jarisch reflex. Am. J. Physiol. 221 (5): 1464-1469. 1971.-The Bezold-Jarisch reflex originates in the left ventricle and produces sinus bradycardia and arterial hypotension. Although it is known that the reflex is mediated via the vagus nerve, its intracardiac route is not known. Our experiments considered three possible afferent routes from the left ventricle: 1) in company with the coronary veins to the coronary sinus and egress from the heart there, 2) in company with the Purkinje system to the left septal endocardium and then via the His bundle back to the coronary sinus, 3) in company with the coronary arteries to the root of the aorta. By cannulating the distal left circumflex artery, selective perfusion with 2 y0 xylocaine blocked the first route; by cannulating the septal artery, selective perfusion with xylocaine blocked the second route; by periarterial infiltration with xylocaine around the main left coronary artery, the third route was blocked. Both the first procedures produced AV block, but none of the three procedures altered normal sinus node responsiveness to vagal stimulation (direct or reflex). Twenty-six dogs were anesthetized with sodium pentobarbital, and the reflex regularly elicited with injection of nicotine into the left anterior descending artery. In 10 dogs the production of local anesthesia and AV block by direct perfusion into the distal left circumflex artery failed to alter the reflex sinus bradycardia. In 11 dogs the production of anesthetic AV block by direct perfusion into the septal artery failed to alter the reflex sinus bradycardia. In four dogs xylocaine anesthesia in both sites still failed to eliminate the reflex. Local infiltration of xylocaine around the main left coronary artery in seven dogs blocked the reflex in all seven. We conclude that the intracardiac route of the Bezold-Jaris& reflex funnels toward the origin of the main left coronary artery for egress from the heart. experimental AV block; reflex sinus bradycardiaTHE BEZOLD-JARISCH REFLEX has beenknown for about 100 years (2, 19, 20, 24). Its principal cardiovascular components are bradycardia and arterial hypotension. Although long familiar to physiologists and pharmacologists, it has generally been considered an oddity of the experimental laboratory. However, bradycardia and hypotension are a frequent clinical observation during acute posterior myocardial infarction in man, and these often (but not always) respond dramatically to the administration of atropine, suggesting that they represent a human counterpart to the experimental reflex (1, 10, 11, 16, 28, 30). Characteristically, the experimental reflex is elicited by chemical stimulation of receptors in the left ventricle with either nicotine or veratridine. Although it has been suggested that the reflex is mediated by coronary chemoreceptors (5), Sleight (29) was able to abolish the response to topically applied nicotine by local anesthesia of the left