辣椒素敏感性感觉神经变性可增强急性心肌梗死大鼠的心肌损伤

Guo, Z.; Departments of Anesthesiology, Shanxi Medical University, Second Hospital of Shanxi Medical University, 56 South Xinjian Nan Road, Taiyuan 030001, Shanxi, China; email:guozheng713@yahoo.com

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 6 h 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. Conclusion: 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. © 2011 Elsevier Ireland Ltd.

Departments of Anesthesiology, Shanxi Medical University, Second Hospital of Shanxi Medical University, 56 South Xinjian Nan Road, Taiyuan 030001, Shanxi, China