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Am J Physiol Heart Circ Physiol 280: H216-H221, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 1, H216-H221, January 2001

Vagosympathetic interactions in ischemia-induced myocardial norepinephrine and acetylcholine release

Toru Kawada1, Toji Yamazaki2, Tsuyoshi Akiyama2, Masashi Inagaki1, Toshiaki Shishido1, Can Zheng1, Yusuke Yanagiya1, Masaru Sugimachi1, and Kenji Sunagawa1

1 Department of Cardiovascular Dynamics and 2 Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Osaka 565-8565, Japan

To elucidate the pathophysiological roles of vagosympathetic interactions in ischemia-induced myocardial norepinephrine (NE) and acetylcholine (ACh) release, we measured myocardial interstitial NE and ACh levels in response to a left anterior descending coronary occlusion in the following groups of anesthetized cats: intact autonomic innervation (INT, n = 7); vagotomy (VX, n = 6); local administration of atropine (Atro, n = 6); transection of the stellate ganglia (TSG, n = 5); local administration of phentolamine (Phen, n = 6); and combined vagotomy and transection of the stellate ganglia (VX+TSG, n = 5). The maximum NE release was enhanced in the VX group (141 ± 30 nmol/l, means ± SE, P < 0.05) compared with the INT group (61 ± 12 nmol/l). Neither the Atro (50 ± 24 nmol/l) nor VX+TSG groups (84 ± 25 nmol/l) showed enhanced NE release. The maximum ACh release was unaltered in the TSG and Phen groups compared with the INT group (19 ± 4, 18 ± 4, and 13 ± 3 nmol/l, respectively). These findings indicate that the cardiac vagal afferent but not efferent activity reduced the ischemia-induced myocardial NE release. In contrast, the cardiac sympathetic afferent and efferent activities played little role in the ischemia-induced myocardial ACh release.

cardiac microdialysis; coronary artery occlusion; vagal nerve; sympathetic nerve; cats


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