To determine the time course of efferent sympathetic denervation after transmural myocardial infarction (TMI) and of efferent vagal denervation after transmural or nontransmural myocardial infarction (NTMI), we measured effective refractory periods (ERP) basal and apical to TMI or NTMI in secobarbital-anesthetized, open-chest dogs. In eight dogs with latex-induced TMI, bilateral ansae subclaviae stimulation shortened ERP at all 45 apical and basal test sites before latex injection. After latex injection, ERP shortening was unchanged at all 15 basal sites but was eliminated (≤2 msec shortening) at three apical sites in 5-20 minutes and at 14 of 30 apical sites 30-180 minutes after latex injection. At the remaining 13 apical sites, ERP shortening was not eliminated but attenuated significantly in 5-180 minutes. ERP shortening induced by infused norepinephrine (0.20-0.25 μg/kg/min) did not differ between basal and apical test sites 3-4 hours after latex injection; that is, no supersensitivity occurred. Of six dogs with TMI produced by ligation of multiple coronary arteries without latex injection, ERP shortening induced by efferent sympathetic neural stimulation was eliminated at 10 apical sites in four dogs over a period of 3 hours. At 14 apical sites that did not show denervation in these six dogs, ERP shortening was unchanged. In seven dogs with latex-induced TMI, bilateral vagal stimulation lengthened ERP at all 40 apical and basal test sites before latex injection. Vagally induced ERP lengthening was unchanged at all 13 basal sites after latex injection. ERP lengthening was eliminated (≤1 msec lengthening) at four of 27 apical sites in 5-20 minutes and at 13 apical sites 30-180 minutes after latex injection. At the remaining 10 apical sites, ERP lengthening was not eliminated but decreased significantly 3 hours after latex injection. Of nine dogs with ligation-induced NTMI, five dogs showed elimination of vagally induced ERP lengthening at eight apical sites in 3 hours after ligation. ERP lengthening induced by vagal stimulation was unchanged at all 17 basal sites in nine dogs with NTMI. We conclude that TMI produced by latex injection and ligation of multiple coronary arteries produces heterogeneous loss of efferent sympathetic innervation in noninfarcted apical sites as early as 5-20 minutes after coronary occlusion with more complete denervation occurring over time. Loss of efferent vagal innervation also occurs heterogeneously in 5-20 minutes after coronary occlusion by latex injection (TMI) and by ligation of a diagonal branch (NTMI) and continues with more sites losing effect responsiveness over time.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine