The Effect Of20-HETE On Rat Myocardial In Ischemia-reperfusion Injury Process In Vitro

20-hydroxy eicosane arachidonic acid (20-HETE) is a product of arachidonicacid generated by cytochrome P-450ω-hydroxylase. Our privious study found that20-HETE could induce cardiomyocyte apoptosis through mitochondrial pathway inneonatal rat cardiomyocytes. In this study, Langendorff technology was used toconstruct the rat isolated heart perfusion model, and left ventricular function of thecardiac was analysised by Powerlab/8P systems. As the results, we found that:(1) At the end of reperfusion, adding20-HETE could decrease the heart rate (HR)gradually, whereas the inhintitor of20-HETE (HET0016) would recover the HRsignificantly and sustainedly;(2)20-HETE led left ventricular development pressure (LVDP) decreasedsignificantly after the end of reperfusion, and HET0016rise the LVDP evidently.(3)20-HETE could cause left ventricular end-diastolic pressure (LVEDP)increase significantly,,on the contrary, HET0016resulting in LVEDP was significantlydecreased. Combined anaylsis of HR, LVDP, LVEDP, the result indicated thatexogenous20-HETE could inhibit cardiac function after reperfusion significantly byincreasing coronary vascular tone, and reduce myocardial oxygen supply lead toaggravate myocardial injury, resulting in increased myocardial infarct size. At thesame time, HET0016may improve myocardial ischemia and reperfusion injury, thiseffect is likely caused by inhibition of the synthase of20-HETE.