Role of Autonomic Nervous System in the Pathogenesis of Prinzmetal's Variant Form of Angina
Role of Autonomic Nervous System in the Pathogenesis of Prinzmetal's Variant Form of Angina
复制标题
自主神经系统在 Prinzmetal 变异型心绞痛发病机制中的作用
作者：
H. Yasue;M. Touyama;M. Shimamoto;H. Kato;Satoru Tanaka;F. Akiyama
对10名患有不同类型心绞痛的患者进行了疗效评估：皮下注射乙酰甲胆碱(10毫克)、阿托品(0.7毫克)和肾上腺素(0.7毫克)；静脉注射异丙肾上腺素(20-25毫克/分钟)；在上述三名在检查时有反复自发性发作的患者中，口服阿托品(0.6-1.2毫克)、心得安(30-90毫克)和苯氧苄明(1名患者10毫克)。对所有患者进行了Master‘s三步两步试验和选择性冠状动脉造影术，在检查时有自发性发作的3例患者中，乙酰甲胆碱诱发发作，阿托品抑制发作。肾上腺素诱发发作2例，心得安对发作无抑制作用。苯氧苯甲胺(在一名患者中)抑制了发作。虽然所有患者的心率分别增加到110次/分钟和160次/分钟以上，但马斯特的三两步试验和异丙肾上腺素输注都不是诱发发作的原因。10例患者中有7例冠状动脉造影术正常。结论是，在静息状态下，副交感神经系统的活动增强，刺激交感神经，进而可能通过激活存在于大冠状动脉的α(血管收缩)受体而导致冠状动脉痉挛，从而参与了发作的启动。
In ten patients with Prinzmetal's variant form of angina the effects of various drugs were assessed: subcutaneous injection of methacholine (10 mg), atropine (0.7 mg), and epinephrine (0.7 mg); intravenous infusion of isoproterenol (20-25 &mgr;g/min); and in the three of the above patients who were having recurrent spontaneous attacks at the time of the examination, oral administration of atropine (0.6-1.2 mg), propranolol (30-90 mg), and phenoxybenzamine (10 mg in one patient). Master's triple two-step test and selective coronary arteriography were done on all the patients.In the three patients who were having spontaneous attacks at the time of the examination, the administration of methacholine induced the attacks and that of atropine suppressed the attacks. Epinephrine induced the attacks in two patients and propranolol was without effect in suppressing the attacks. Phenoxybenzamine (in one patient) suppressed the attacks. Neither Master's triple two-step test nor isoproterenol infusion precipitated the attacks, though heart rate increased to more than 110 beats/min and 160 beats/min respectively in all the patients. Coronary arteriograms were normal in seven of the ten patients.It is concluded that enhanced activity of the parasympathetic nervous system, which occurs at rest, is involved in the initiation of the attack by stimulating the sympathetic nerve which in turn probably induces coronary arterial spasm by way of activating alpha (vasoconstrictor) receptors present in the large coronary arteries.