ISCHEMIC REPERFUSION INJURY IN HYPERTENSIVE RAT HEART

Abstract

Objective: In patients with cardiovascular disease, myocardial ischaemia reperfusion damage is the leading cause of death. Sustained myocardial ischaemia–reperfusion causes cardiomyocyte death and coronary microvascular injury in different ways. Patients with hypertension who undergo cardiac ischemia-reperfusion have more severe clinical outcomes. Design and method: The mechanism, on the other hand, is missing. We use an angiotensin II successfully produced hypertension rat model to investigate the effect of hypertension on cardiac ischemia-reperfusion injury. We successfully established in vitro myocardial ischemia-reperfusion in normal and hypertensive rat hearts using the Langendorff perfusion system. Results: Our results reveal that after 30 minutes of ischemia and an hour of reperfusion, the beating pattern of the hypertensive heart was poorer than that of the sham heart. We also used a Transmission Electron Microscope to examine the morphology of myocardial cells and mitochondria, and discovered that the mitondria structure was dramatically destroyed in the hypertension model compared to the sham model, and that some myocytes in the hypertension model have abnormal morphology after 30 minutes of ischemia and an hour of reperfusion. To assess mitochondrial function, mitochondria were extracted from an ischemia-reperfused heart and Mitochondrial Function Indexes were calculated. When oligomycin was used to block ATP synthase, the formation of reactive oxygen species (ROS) and mitochondrial membrane potential MMP increased considerably in the hypertension group. Furthermore, when FCCP was utilized as a proton collapser and antimycin A was used to block mitochondrial complex III, the generation of reactive oxygen species (ROS) mitochondrial membrane potential MMP in the hypertension group rose significantly at add additional oil substrate. When the hypertension group is given the substrate succinate or oligomycin to block ATP synthase, oxygen consumption increases significantly. Conclusions: Taken together, our research reveals that hypertension can significantly increase the damage caused by myocardial ischemia reperfusion. As a result, hypertension during myocardial ischemia should be given special attention.