title: Postischemic deterioration of sarcoplasmic reticulum: warm versus cold blood cardioplegia.
abstract: Impaired cardiac sarcoplasmic reticulum (SR) function, as evidenced by reduced SR Ca2+ uptake rate and decreased SR Ca(2+)-adenosine triphosphatase activity, has been found in postischemic "stunned" myocardium and in hearts subjected to hypothermic arrest. In this study, we compared the effects of retrograde continuous coronary sinus warm blood cardioplegia (WBC) and retrograde intermittent cold blood cardioplegia (CBC) on cardiac SR function and postischemic ventricular functional recovery in pig hearts. Twelve in situ isolated pig hearts supported by cardiopulmonary bypass were subjected to 120 minutes of cardioplegic arrest with either WBC (37 degrees C) or CBC (6 degrees to 10 degrees C), followed by 60 minutes of 37 degrees C reperfusion. Left ventricular global contractile function and coronary blood flow were measured before arrest and during reperfusion. Cardiac SR was isolated from left ventricular biopsy specimens, and 45Ca2+ uptake by SR and SR Ca(2+)-adenosine triphosphatase activity were determined. The recovery of left ventricular global contractile function as indicated by the maximum of the first derivative of left ventricular pressure was significantly improved in the WBC group compared with that of the CBC group (70% versus 46%; p < 0.05). The SR Ca(2+)-adenosine triphosphatase activity was better preserved after 60 minutes reperfusion in WBC compared with CBC (0.31 +/- 0.02 versus 0.20 +/- 0.03 microM Pi/min/mg protein, p < 0.05), and the recovery of SR Ca2+ uptake was significantly improved by WBC compared with CBC (1.15 +/- 0.12 versus 0.83 +/- 0.04 microM Ca2+/min/mg protein; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Surgery, University of Connecticut School of Medicine, Farmington.
authors.forename: X
authors.initials: X
authors.lastname: Liu
authors.forename: R M
authors.initials: RM
authors.lastname: Engelman
authors.forename: Z
authors.initials: Z
authors.lastname: Wei
authors.forename: N
authors.initials: N
authors.lastname: Maulik
authors.forename: J A
authors.initials: JA
authors.lastname: Rousou
authors.forename: J E
authors.initials: JE
authors.lastname: Flack
authors.forename: D W
authors.initials: DW
authors.lastname: Deaton
authors.forename: D K
authors.initials: DK
authors.lastname: Das
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D002118:Calcium / Q000493:pharmacokinetics; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D002314:Cardioplegic Solutions; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D006324:Heart Arrest, Induced; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology* / Q000601:surgery; D012519:Sarcoplasmic Reticulum / Q000378:metabolism / Q000502:physiology*; D013552:Swine; D013696:Temperature; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology
chemical_list: D002314:Cardioplegic Solutions; D003402:Creatine Kinase; D000252:Calcium-Transporting ATPases; D002118:Calcium