title: [Effects of verapamil preconditioning on cardiac function in vitro and intracellular free Ca2+ and L-type calcium current in rat cardiomyocytes post ischemia-reperfusion injury].
abstract: OBJECTIVE
  To investigate the influences of verapamil preconditioning on cardiac function in vitro and intracellular free Ca2+ and L-type calcium current (I(Ca-L)) in rat cardiomyocytes post ischemia-reperfusion (I/R) injury.
  
  
  METHODS
  The isolated rat hearts in control group (37 degrees C Tyrode solution perfusion for 30 min, n = 6), I/R group (no flow for 30 min followed 30 min reperfusion with 37 degrees C Tyrode solution, n = 7) and verapamil preconditioning group [37 degrees C Tyrode solution perfusion for 10 min, adding verapamil (20 micromol/L) to Tyrode solution and perfusion for another 30 min, followed then by 30 min no flow and 30 min reperfusion, n = 7] using Langendorff perfusion system. The fluorescence intensity of intracellular Ca2+ was detected with Fluo-3/AM loading by the laser scanning confocal microscope. The I(Ca-L) was recorded via whole-cell patch clamp technique in enzymatically dissociated single rat ventricular myocytes.
  
  
  RESULTS
  As expected, arrhythmias and cardiac dysfunction were shown post I/R injury. The fluorescence intensities of intracellular free Ca2+ in cardiomyocytes were significantly increased compared with control group (P < 0.01). By voltage clamp protocol, peak current densities of I(Ca-L) was significantly reduced and I-V curve significantly elevated. Post I/R injury compared with control group (P < 0.01) which could be reversed by Verapamil preconditioning. Verapamil preconditioning also significantly improved diastolic and systolic functions, and reduced the incidence of arrhythmias.
  
  
  CONCLUSIONS
  Myocardial I/R injury might significantly impair heart functions and induce arrhythmias via cellular Ca2+ overload. Verapamil preconditioning could prevent heart I/R injury and reduce arrhythmias by decreasing influx of I(Ca-L), thereby stabilizing cardiomyocytes in myocardial stunning and avoiding occurrence of Ca2+-induced Ca2+ release during I/R injury.
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Yu
authors.forename: Jing-Jing
authors.initials: JJ
authors.lastname: Wang
authors.forename: Wen-Yun
authors.initials: WY
authors.lastname: Gan
authors.forename: Guo-Sheng
authors.initials: GS
authors.lastname: Lin
authors.forename: Cong-Xin
authors.initials: CX
authors.lastname: Huang
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D020746:Calcium Channels, L-Type / Q000187:drug effects; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014700:Verapamil / Q000494:pharmacology*
chemical_list: D020746:Calcium Channels, L-Type; D014700:Verapamil; D002118:Calcium