Effect of ischemic preconditioning on myocardial protection in rat heart

Abstract

Background: Ischemic preconditioning, direct or remote, has been known to protect the myocardium against lethal ischemic injury. Expression of neural cell adhesion molecule (NCAM) is also known to have protective and regulating effects on myocardial infarction. The aims of the present study are

(1) to compare the effect of direct versus remote type of ischemic preconditioning on myocardial protection, (2) to examine the expression level of neural cell adhesion molecule (NCAM) in acute stage of myocardial infarction, and (3) to demonstrate if the expression of NCAM is involved in myocardial ischemic preconditioning models in rat. Methods: Ischemic preconditioning was induced in Sprague-Dawley (SD) rat by three cycles of 3 minutes occlusion of the left anterior descending coronary artery (Direct group, n=7) or left femoral artery (Remote group, n=7), followed by 5 minutes of reperfusion. Myocardial ischemia was produced by ligation of the left anterior descending coronary artery for 50 minutes, followed by reperfusion for 50 minutes (Control group, n=7). Infarct and at risk area was determined by 2,3,5-triphenyltetrazolium chloride staining. Immunohistochemistry was performed with anti-NCAM rabbit polyclonal antibody H-300. Expression level of NCAM of infarct area was presented as the ratio of intensity of infarct area to intensity of the reference area. Results: The direct ischemic preconditioning significantly decreased the infarct size (p = 0.003) when compared with that of the control group. The infarct size was also decreased in the remote group, however, there was no significant difference when compared with that of the control group (p = 0.269). The infarct size in the direct group was smaller than that in the remote group without significant difference between two groups (p = 0.097). In the immunohistochemistry, the expression of NCAM in the direct group was lower than the other 2 groups

however, there was no significant difference in the NCAM expression level among the three groups. Conclusions: Ischemic preconditioning to the left anterior descending coronary artery territory provided a myocardial protection for ischemia-reperfusion injury to the same coronary artery territory. However, the protective effect of ischemic preconditioning to the femoral artery was not significant in the rat myocardium infarction model. The expression of NCAM seemed to be down-regulated in the acute stage of myocardial infarction and showed no differences in the groups of ischemic preconditioning in rat.