title: Normothermic versus hypothermic hyperkalemic cardioplegia: effects on myocyte contractility.
abstract: BACKGROUND
  This study was designed to determine the effects of prolonged hyperkalemic cardioplegic arrest under normothermic or hypothermic conditions with respect to left ventricular myocyte contractile performance and beta-adrenergic responsiveness.
  
  
  METHODS
  Isolated left ventricular porcine myocytes were randomly assigned to one of three groups: (group 1) normothermic control, (group 2) hypothermic cardioplegic arrest, or (group 3) normothermic cardioplegic arrest. Myocyte contractility was evaluated by high-speed video microscopy at baseline and after beta-adrenergic stimulation with isoproterenol (25 nmol/L).
  
  
  RESULTS
  Myocyte velocity of shortening was decreased after both hypothermic and normothermic cardioplegic arrest (68 +/- 2 and 69 +/- 2 microns/s, respectively) compared with normothermic control values (96 +/- 2 microns/s; p < 0.05). This relative reduction in baseline contractile function was equivalent in both cardioplegia groups (p = 0.5356). With beta-adrenergic stimulation, myocyte velocity of shortening was 186 +/- 4 microns/s in the hypothermic and 176 +/- 3 microns/s in the normothermic cardioplegia groups (p = 0.0563). However, myocyte contractility with beta-adrenergic stimulation was reduced in both cardioplegia groups compared with normothermic controls (205 +/- 4 microns/s; p < 0.05, respectively).
  
  
  CONCLUSIONS
  Hyperkalemic cardioplegic arrest under either normothermic or hypothermic conditions resulted in an equivalent reduction in baseline myocyte contractile function with reperfusion/rewarming. Hypothermic cardioplegic arrest may have provided mild protective effects on beta-adrenergic responsiveness. Nevertheless, these results suggest that an important contributory factor for diminished myocyte contractility after simulated cardioplegic arrest was prolonged exposure to a hyperkalemic environment.
authors.affiliation: Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston 29425, USA.
authors.forename: W V
authors.initials: WV
authors.lastname: Houck
authors.forename: S B
authors.initials: SB
authors.lastname: Kribbs
authors.forename: J L
authors.initials: JL
authors.lastname: Zellner
authors.forename: M A
authors.initials: MA
authors.lastname: Doscher
authors.forename: J D
authors.initials: JD
authors.lastname: Joshi
authors.forename: F A
authors.initials: FA
authors.lastname: Crawford
authors.forename: F G
authors.initials: FG
authors.lastname: Spinale
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D001831:Body Temperature; D002314:Cardioplegic Solutions / Q000627:therapeutic use*; D002478:Cells, Cultured; D006324:Heart Arrest, Induced; D006982:Hypertonic Solutions / Q000627:therapeutic use*; D007036:Hypothermia, Induced; D007545:Isoproterenol / Q000494:pharmacology; D018715:Microscopy, Video; D009200:Myocardial Contraction / Q000187:drug effects*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000166:cytology; D017680:Potassium Compounds / Q000627:therapeutic use*; D011897:Random Allocation; D017694:Rewarming; D013552:Swine; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000318:Adrenergic beta-Agonists; D002314:Cardioplegic Solutions; D006982:Hypertonic Solutions; D017680:Potassium Compounds; C018369:potassium cardioplegic solution; D007545:Isoproterenol