title: [The effects of diazoxide on myocardium function and the expressions of ERK and JNK in isolated spontaneous hypertension rat hearts].
abstract: OBJECTIVE
  To investigate the effect of diazoxide preconditioning and the role of ERK and JNK in cellular signaling during diazoxide preconditioning protection in isolated spontaneous hypertension rat (SHR) hearts.
  
  
  METHODS
  Hearts were isolated from male SHR rats, and perfused on a Langendorff apparatus. Five groups were considered (n = 6). Con: after 40 min perfusion the hearts were submitted to 25 min ischemia followed by 30 min reperfusion. IP: the hearts were preconditioned with 2 periods of 5 min ischemia and 10 min reperfusion prior to 25 min ischemia. DP: the hearts were preconditioned with 2 periods of 10 min K-H solution with 50 micromol x L(-1) diazoxide and 5 min K-H solution reperfusion prior to 25 min ischemia. 5-HD: perfuse with 100 micromol x L(-1) 5-HD (a special mitochondrial ATP sensitive potassium channel blocker) for 10 min followed by 30 min K-H solution perfusion before 25 min ischemia. 5-HD + DP: 100 micromol x L(-1) 5-HD was given for 10 min before diazoxide preconditioning.
  
  
  RESULTS
  During reperfusion, comparing with Con group, the recoveries of left ventricle developed pressure (LVDP), + dP/dt(max), - dP/dt(max) and left ventricle end diastolic pressure (LVEDP) were improved in IP and DP groups (P < 0.01 vs Con). At the end of reperfusion, compared with Con group, the expression of ERK in myocardium were higher in IP and DP groups (P < 0.01 vs Con), there was no significance between 5-HD and Con group, but 5-HD couldn't inhibit the expression of ERK induced by diazoxide preconditioning. The expression of JNK in IP and DP groups were decreased (P < 0.05 vs Con), this effect could been inhibited by 5-HD.
  
  
  CONCLUSIONS
  These results indicated that diazoxide preconditioning could mimic ischemic preconditioning, the activation of ERK expression and the declining of JNK expression involved in diazoxide preconditioning in isolated SHR hearts.
authors.affiliation: Department of Anesthesiology, The 2nd Affiliated Hospital of Wenzhou Medical College, Wenzhou 325027, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Cao
authors.forename: Xiu-Xia
authors.initials: XX
authors.lastname: Chen
authors.forename: Bo
authors.initials: B
authors.lastname: Gui
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.forename: Shi-Ming
authors.initials: SM
authors.lastname: Duan
authors.forename: Yin-Ming
authors.initials: YM
authors.lastname: Zeng
mesh_terms: D000818:Animals; D003981:Diazoxide / Q000494:pharmacology*; D066298:In Vitro Techniques; D048670:MAP Kinase Kinase 4 / Q000378:metabolism; D020935:MAP Kinase Signaling System; D008297:Male; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR
chemical_list: D048670:MAP Kinase Kinase 4; D003981:Diazoxide