Abstract

Introduction: Caveolin-1 (Cav-1) is the main structural protein of caveolae, which is dominantly expressed in vascular tissue. It associates with vascular homeostasis by regulating vascular signals. However, Cav-1 KO aggravated the cardiac dysfunction of systolic and diastolic function after cardiac ischemia reperfusion. Injection of Cav-1 peptides successfully preserved left ventricular function post-ischemic reperfusion through the increase in nitric oxide (NO). Hypothesis and Methods: To evaluate the role of Cav-1 in cardiac function, we assessed cardiac function, heart rate and coronary artery blood flow through global ischemia and reperfusion using Langendorff-perfused mouse heart model. Results: In the final analysis of 15 mice, 7 were wild type (WT) and 8 were Cav-1 KO at the age of 12-23 weeks. There are significantly differences in baseline of Left ventricular pressure (LVP), heart rate (HR), max and minimum dp/dp before and after ischemia in each mouse group. We further concluded that the markedly decrease of Coronary artery flow (CF) is the reason for the inhibition of cardiac diastolic function, while heart rate (HR) did not show obvious difference in WT and Cav-1 KO mice. Cav-1 deficiency inhibited the coronary artery flow after ischemia reperfusion and led to aggravation of cardiac dysfunction. Conclusions: As further experiments are needed, both cardiac functions and coronary flow in Cav-1 KO could be impaired. More experiments will be performed and results will be updated.

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