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

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... usions of the left anterior descending coronary artery (LAD) followed by 60-min reperfusion abolished electrical stimulation-induced ACh release (20.4 Ϯ 3.9 vs. 0.9 Ϯ 0.4 nmol/l; means Ϯ SE, P Ͻ 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 Ϯ 1.8 vs. 3.9 Ϯ 0.7 nmol/l; P Ͻ 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 AUTONOMIC DERANGEMENT ASSOCIATED with acute myocardial ischemia or infarction has deleterious effects on the heart (3, 6). The autonomic derangement occurs during postischemic as well as ischemic periods. Elucidating the underlying mechanisms of autonomic disturbance during the postischemic period is important to understand the pathophysiology of postischemic events such as those occurring after thrombolytic therapies. In the sympathetic nervous system, nerve terminal function as assessed by tyramine-induced norepinephrine release recovers 60-120 min after reperfusion of the coronary artery (1, 14) . On the other