INTERRUPTION OF SYMPATHETIC AND VAGAL-MEDIATED AFFERENT RESPONSES BY TRANSMURAL MYOCARDIAL-INFARCTION
INTERRUPTION OF SYMPATHETIC AND VAGAL-MEDIATED AFFERENT RESPONSES BY TRANSMURAL MYOCARDIAL-INFARCTION
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DOI：
10.1161/01.cir.72.3.623
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发表时间：
1985-01-01
期刊：
影响因子：
37.8
通讯作者：
ZIPES, DP
中科院分区：
文献类型：
--
作者：
BARBER, MJ;MUELLER, TM;ZIPES, DP
交感神经和迷走神经传入在心脏中以从顶端到基底的过程传播，并且可以分别通过心外膜应用缓激肽和尼古丁选择性地刺激。测试了透壁性心肌梗塞 (TMI) 中断穿过梗塞的交感神经和迷走神经传入纤维并在梗塞顶端区域产生传入去神经支配区域的假设。在开胸、氯醛糖麻醉的狗中，通过将乙烯基乳胶溶液直接注射到动脉中并迅速硬化，栓塞左冠状动脉前降支的对角分支，从而产生 TMI。通过脱氢酶硝基蓝四唑染色技术验证梗塞的透壁性质。心外膜应用缓激肽（5μg）和尼古丁（50μg）分别用于刺激化学敏感的交感神经和迷走神经传入神经末梢。在 TMI 产生之前和之后 90 分钟对 29 只狗进行了研究。在 20 只狗中，在产生 TMI 之前应用心外膜缓激肽，产生了 13 .+- 的最大升压反应。应用后 40 秒为 3 mm Hg（与应用前值相比，P < .01），而局部尼古丁产生的最大抑制反应为 14 .+-。 2 mm Hg（P < .01 与应用前值相比） 在所有测试地点应用后 20 秒。 TMI 产生后 90 分钟，梗塞基底的心外膜部位继续对两种药物产生正常反应，而梗塞区域内的部位和该区域的心尖部位（非梗塞心肌）不再表现出对局部缓激肽的升压反应或对局部尼古丁的降压反应。对 12 只狗的神经中断表明，缓激肽引起的交感传入反应可以通过双侧星状切除术消除，而尼古丁引起的迷走神经传入反应则可以通过横断颈部迷走神经来中断。在 10 只狗中，对两种药物的反应进行更广泛的心外膜绘图显示，这些部位并不总是以均匀的方式去传入神经。 TMI 内侧和顶端的几个部位继续表现出对缓激肽的升压反应，但对局部尼古丁没有反应。 TMI 在梗塞区和梗塞区心尖部的非梗塞心肌中产生交感神经和迷走神经传入去神经支配区域。这种传入去神经支配并非在所有区域都是均匀的。
Sympathetic and vagal afferents travel in an apical-to-basal course in the heart and can be stimulated selectively with epicardial applications of bradykinin and nicotine, respectively. The hypothesis that transmural myocardial infarction (TMI) interrupts sympathetic and vagal afferent fibers traveling through the infarction and produces regions of afferent denervation in areas apical to the infarction was tested. In open-chest, chloralose-anesthetized dogs TMI was created by embolizing a diagonal branch of the left anterior descending coronary artery with a vinyl latex solution that was injected directly into the artery and hardened rapidly. The transmural nature of the infarction was verified by the nitro blue tetrazolium staining technique for dehydrogenase enzymes. Epicardial applications of bradykinin (5 .mu.g) and nicotine (50 .mu.g) were used to stimulate chemically sensitive sympathetic and vagal afferent nerve endings, respectively. Twenty-nine dogs were studied before and 90 min after creation of TMI. In 20 dogs, epicardial bradykinin applied before production of TMI produced a maximal pressor response of 13 .+-. 3 mm Hg 40 s after application (P < .01 vs. preapplication values), while topical nicotine produced a maximal depressor response of 14 .+-. 2 mm Hg (P < .01 vs. preapplication values) 20 s after application at all sites tested. Ninety min after production of TMI, epicardial sites basal to the infarction continued to respond normally to both drugs, while sites within the area of infarction and apical to the area (noninfarcted myocardium) no longer showed a pressor response to topical bradykinin or a depressor response to topical nicotine. Nerve interruptions in 12 dogs demonstrated that the sympathetic afferent responses elicited by bradykinin were eliminated with bilateral stellectomy, while vagal afferent responses elicited by nicotine were interrupted by transection of the cervical vagi. In 10 dogs, more extensive epicardial mapping of responses to the 2 drugs revealed that sites were not always afferently denervated in a homogeneous manner. Several sites medial and apical to the TMI continued to show pressor responses to bradykinin, but were unresponsive to topical nicotine. TMI produces areas of both sympathetic and vagal afferent denervation in infarcted and in noninfarcted myocardium apical to the region of infarction. This afferent denervation is not homogeneous in all areas.