Degeneration of capsaicin sensitive sensory nerves enhances myocardial injury in acute myocardial infarction in rats.

BACKGROUND

Evidence indicated an involvement of afferent nerves in the pathology of acute myocardial infarction. This study was undertaken to clarify the role and mechanisms by which the sensory afferent degeneration exacerbates the myocardial injury in acute myocardial infarction in rats.

METHODS

The myocardial injury was assessed by analysis of 1) the differences in the infarct size, myocyte apoptosis, the caspase activity in the myocardium and cardiac troponin I in serum between the denervated and non-denervated rats; 2) the differences in the size of infarctiom with and without antagonisms of endogenous neurokinin 1 receptor or calcitonin gene related peptide receptor in acute myocardial infarction.

RESULTS

Degeneration of the afferent nerves resulted in marked increase in the pain threshold and decrease in substance P and calcitonin gene related peptide in dorsal root ganglia, spinal dorsal horn and myocardium. Increases of the infarction size (39% ± 4% vs. 26% ± 4%,), troponin-I (28.4 ± 8.89 ng/ml, vs. 14.6 ± 9.75 ng/ml), apoptosis of myocytes (by 1.8 ± 0.2 folds) and caspase-3 activity (1.6 ± 0.3 vs. 1.05 ± 0.18) were observed in the denervated animals at 6h of myocardial infarction, compared with the non-denervated rats. Antagonisms of the endogenous neurokinin 1 receptor or calcitonin gene related peptide receptor caused increase of the size of infarction in the animals.

CONCLUSIONS

Degeneration of capsaicin sensitive afferent nerves enhances the myocardial injury of acute myocardial infarction, possibly due to reduction of endogenous calcitonin gene related peptide and substance P.