title: Improvement of ventricular mechanical properties by puerarin involves mitochondrial permeability transition in isolated rat heart during ischemia and reperfusion.
abstract: The aim of the present study was to determine whether the clinically effective cardioprotection conferred by puerarin (Pue) against ischemia and reperfusion is mediated by mitochondrial transmembrane pores and/or channels. In isolated rat hearts subjected to 30 min regional ischemia and 120 min reperfusion, pretreatment with Pue at 0.24 mmol/L for 5 min before ischemia increased myocardial formazan content, an index of myocardial viability, reduced lactate dehydrogenase release, improved recovery of the maximal rise/fall rate of left ventricular pressure, left ventricular end-diastolic pressure and rate-pressure product (left ventricular developed pressure multiplied by heart rate) during reperfusion. Administration of atractyloside (20 micromol/L), an opener of the mitochondrial permeability transition pore, for the first 20 min of reperfusion and 5-hydroxydecanoate (100 micromol/L), the mitochondrial specific ATP-sensitive potassium channel blocker, for 20 min before ischemia, attenuated the protective effects of Pue. In mitochondria isolated from hearts pretreated with 0.24 mmol/L Pue for 5 min, a significant inhibition of Ca2+-induced swelling was observed, and this inhibition was attenuated by 5-hydroxydecanoate. These findings indicate that Pue protects the myocardium against ischemia and reperfusion injury via inhibiting mitochondrial permeability transition pore opening and activating the mitochondrial ATP-sensitive potassium channel.
authors.affiliation: Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China qin@zju.edu.cn.
authors.forename: Qin
authors.initials: Q
authors.lastname: Gao
authors.forename: Hong-Yang
authors.initials: HY
authors.lastname: Pan
authors.forename: Iain C
authors.initials: IC
authors.lastname: Bruce
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xia