The Protection Of Nitric Oxide And Nitric Oxide Synthas To Myocardium

Objective:To investigate the production level of nitric oxide(NO) and nitric oxide synthas (NOS) activity on Ischemia-reperfusion and Ischemia postconditioning to myocardial. Lactate dehydrogenase(LDH) activity and myocardial infarct size were observed after using excitomotory and inhibitory of NOS. To approach protection of NO and nitric oxide synthas (NOS) to ischemia postconditioning.MethodsForty-eight Wistar rats were randomly divided into four groups:control group,experiment group,excitomotory group and inhibitory group. Isolated rat hearts were mounted on a Langendorff perfusion apparatus. Control group, isolated rat hearts were perfused with Kreb's perfusion buffer and maintained for 10 min of heart working, ischemia for 30 min and reperfused for 120 min. In experiment group the isolated hearts were subjected to three cycles of 30 s followed by 30 s re-occlusion immediately upon 117 min. Excitomotory group (Ischemia-reperfusion+L-Arg) stopped blood-supply for 30 min and reperfused for 120 min. Perfusion buffer was Kreb's contained lmmol/L L-Arg. In inhibitory group, isolated rat hearts were perfused with Kreb's perfusion buffer contained lmmol/L L-NNA and subjected to three cycles of 30 s R followed by 30 s re-occlusion immediately upon 117 min.After the reperfusion, NO content in the perfusion fluid and the activity of NOS were assayed by HPLC. The myocardial infarct size was determined by the TTC staining method. The LDH activity was determined by ultraviolet spectrophotometry.Results1. Contrast of LDH activity and infarct size between Ischemia-reperfusion and Ischemia postconditioning.The LDH activity in experiment group was lower than that in control group (P< 0.01).The myocardial infarct size in experiment group was less than that in control group (P<0.05).2. Contrast of NOS activity and the production level of NO between Ischemia-reperfusion and Ischemia postconditioning.Both the NOS activity and the production level of NO in experiment group were higher than that in control group (P<0.05).3. Effects of excitomotory and inhibitory of NOS to myocardium.NO content in both the experiment group and the inhibitory group were significantly higher than that in the control group (P<0.05),There was statistic differences between the control group and the excitomotory group on the NO content (P<0.05).Activity of NOS in the experiment group was significantly higher than that in the excitomotory group and the inhibitory group (P<0.05).The LDH activity and the myocardial infarct size in the experiment group, the inhibitory group and the excitomotory group were significantly lower than those in the control group (P<0.05).There was statistic differences between the experiment group and the inhibitory group on the LDH activity and the myocardial infarct size (P<0.05).Conclusions1. Ischemia postconditioning can reduce the myocardial infarct size and the LDH release of myocardial cells. Consequently, Ischemia postconditioning can protect ischemia-reperfused myocardium.2. Because of protection to myocardial cells, the quantity of eNOS on the endothelial cells in postconditioning is more than in reperfused. Consequently, Both the NOS activity and the production level of NO in postconditioning are higher than that in reperfused,3. Both the NOS activity and the production level of NO in postconditioning are higher than those in reperfused. And the degree of myocardial damage in postconditioning is lower than that in reperfused. After using inhibitory of NOS, the protection of ischemia postconditioning to myocardial cells is degraded. Using excitomotory of NOS can reduce myocardial damage in ischemia-reperfused.4. The results of this study indicate that using excitomotory of NOS like L-Arg can increase the NOS activity and the production level of NO, at the same time myocardium is protected. But inhibitory of NOS like L-NNA not only reduce the production level of NO and the NOS activity, but also relax the protection of postconditioning to myocardial. Accordingly, we conjecture that NO play an action in the protection of postconditioning mechanism to myocardial. NOS excitomotory can protect ischemia-reperfused myocardium. The findings might provide new basic information for further researches on healing myocardial infarction patients in clinical.