Cardiovascular diseases are very harmful to human life and health. Reperfusion
therapy is a standard method to treat
cardiovascular diseases and has achieved high clinical effects. However, this treatment method is likely to cause
myocardial ischemia-
reperfusion injury. It has been reported that the
Rho kinase inhibitor
fasudil can interfere with cardiomyocyte apoptosis through the Rho-ROCK signaling pathway, so it is often used to treat
cardiovascular diseases. The essay aims to research this specific influence of
fasudil on cardiac damage in
myocardial ischemia-reperfusion mouses through the Rho-ROCK signal path and its related mechanisms. Forty rats were taken as the research object, and the mouses were separated into control clusters. In the observation cluster of
fasudil, the rat heart device was perfused by surgery. The rat coronary artery was ligated for 20 minutes to make the rat
myocardial ischemia. Then, the
ligation was loosened for myocardial perfusion to create a rat
myocardial ischemia-reperfusion model. Observation group rats were perfused with quantitative
fasudil, 80 minutes after
ischemia-reperfusion, the ultrastructural changes and myocardial ischemic area of the rat myocardium were observed under a microscope, and the dynamic changes of the mouse heart were examined by flow cytometry. The PCR fluorescence method was used to explore the outlook layer of Rho-ROCK
kinase activity to detect rat cardiomyocyte apoptosis. It is shown that under this intervention of
fasudil, this expression level of Rho-ROCK
kinase activity in the observation group was reduced by 18.3%, the myocardial cell apoptosis rate was decreased by 26.4%, and one area of
myocardial ischemia can be reduced by 32.5%. The ultrastructure of the new object in rats is improved, and the left ventricular diastolic and systolic effect is enhanced. Therefore, the
fasudil may decrease cardiac
ischemia and focus on injured Rho-ROCK signal path activity.