Acute transmural
myocardial infarction has been reported to functionally denervate the normal myocardium distal to the infarcted zone by interrupting neurotransmission in axons coursing in the subepicardial region of the myocardial
necrosis. To directly investigate the viability of such neurotransmission, the effects of acute transmural
myocardial infarction on conduction in the intrinsic cardiac nerves overlying and distal to an experimentally induced acute transmural
myocardial infarction were studied. In eight dogs, during control states electrical stimulation of the epicardium adjacent to a coronary artery produced compound action potentials in the more cranially located cardiopulmonary nerves. Thereafter, in four dogs an acute transmural
myocardial infarction was produced by injecting rapidly hardening
latex into a major diagonal branch of the left anterior descending coronary artery. Epicardial stimulation over the
infarct, as well as proximal or distal to it, produced compound action potentials that conducted at normal velocities for at least 12 h postinfarction. The transmural extent of the
infarct was verified with
tetrazolium blue staining at the end of the experiment. In the other four
dogs, compound action potentials were generated in cardiopulmonary nerves as described above and then
ventricular fibrillation was produced to assess the effects of global
anoxia on the function of axons coursing in cardiac nerves. Following the onset of
ventricular fibrillation, compound action potentials were generated in these nerves in C fibers for up to 2 h, in B fibers for up to 4 h, and in A fibers for at least 12 h.(ABSTRACT TRUNCATED AT 250 WORDS)