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Am J Physiol Heart Circ Physiol 283: H2687-H2691, 2002. First published August 29, 2002; doi:10.1152/ajpheart.00291.2002
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Vol. 283, Issue 6, H2687-H2691, December 2002

Disruption of vagal efferent axon and nerve terminal function in the postischemic myocardium

Toru Kawada1, Toji Yamazaki2, Tsuyoshi Akiyama2, Hidezo Mori2, Kazunori Uemura1, Tadayoshi Miyamoto1, Masaru Sugimachi1, and Kenji Sunagawa1

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

Despite the importance of vagal control over the ventricle, little is known regarding vagal efferent conduction and nerve terminal function in the postischemic myocardium. To elucidate postischemic changes in the cardiac vagal efferent neuronal function, we measured myocardial interstitial acetylcholine (ACh) levels by using in vivo cardiac microdialysis and examined the ACh responses to electrical stimulation of the vagi or local administration of ouabain in anesthetized cats. Sixty-minute occlusions of the left anterior descending coronary artery (LAD) followed by 60-min reperfusion abolished electrical stimulation-induced ACh release (20.4 ± 3.9 vs. 0.9 ± 0.4 nmol/l; means ± SE, P < 0.01). In different groups of animals, 60-min LAD occlusion followed by 60-min reperfusion decreased but did not completely abolish ouabain-induced release of ACh (9.2 ± 1.8 vs. 3.9 ± 0.7 nmol/l; P < 0.05). These results indicate that function of the vagal efferent axon was completely interrupted, whereas the local ACh release was partially suppressed in the postischemic myocardium. The postischemic disruption of vagal efferent neuronal function might exert deleterious effects on cardiac regulation.

cardiac microdialysis; vagal stimulation; ouabain; cats; acetylcholine


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