title: Effect of pinacidil on rat ventricular myocytes during transient hypoxia and reperfusion.
abstract: The aim of this study was to evaluate the cardioprotective effect of pinacidil postconditioning on rat hearts with transient hypoxia and reperfusion. An acute myocardial anoxia-reperfusion rat model was created by ligating coronary arteries for 10 min and subsequent reperfusion for 60 min. Twenty-four rats in 4 groups received different treatments: normal hearts as control (N = 6), anoxia-reperfusion (A/R) only (N = 6), pinacidil postconditioning (N = 6), and pinacidil plus adenosine triphosphate-sensitive potassium channel inhibitors (glibenclamide) (N = 6). The kinetic parameters and electrophysiological properties, including early apoptosis protein expression changes of Bax, Bcl-2, and FN were examined using the isolated perfusion and patch-clamp technique and immunohistochemistry. The left ventricular systolic pressure and maximum -dp/dt in A/R groups were significantly higher than those in the control group (P < 0.05). The left ventricular developing pressure, maximum +dp/dt, and heart rate in the A/R group were slightly decreased. The pinacidil-postconditioned group has better cardiac function recovery after ischemia/reperfusion than the A/R group (P < 0.01). In addition, using the patch-clamp technique, the mean open time and conductance values are significantly higher in the pinacidil postconditioning group, compared with those in the A/R group. The expression of apoptosis proteins (Bax, FN) increased during A/R, while Bcl-2 protein expression decreased. A significant difference was found in the pinacidil treatment group relative to the A/R group. Pinacidil postconditioning can exert cardioprotective effects on A/R-injured rat hearts, which may indicate a potential application of pinacidil postconditioning to protect A/R-injured hearts.
authors.affiliation: Department of Cardiology, Wuhan Third Hospital & Affiliated Tongren Hospital, Medical College, Wuhan University, China.
authors.forename: X Y
authors.initials: XY
authors.lastname: Dong
authors.affiliation: Department of Cardiology, Wuhan Third Hospital & Affiliated Tongren Hospital, Medical College, Wuhan University, China fenzhucn@126.com.
authors.forename: F
authors.initials: F
authors.lastname: Zhu
mesh_terms: D000818:Animals; D017209:Apoptosis; D006352:Heart Ventricles / Q000187:drug effects* / Q000378:metabolism*; D000860:Hypoxia; D008297:Male; D023421:Models, Animal; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism*; D020110:Pinacidil / Q000008:administration & dosage / Q000494:pharmacology*; D015221:Potassium Channels / Q000378:metabolism; D051381:Rats; D014665:Vasodilator Agents / Q000494:pharmacology; D016277:Ventricular Function, Left
chemical_list: D015221:Potassium Channels; D014665:Vasodilator Agents; D020110:Pinacidil