title: Perfusion delay causes unintentional ischemic preconditioning in isolated heart preparation.
abstract: This study sought to show that unintentional preconditioning can be induced in the isolated perfused heart during the preparation procedure. The following four groups were compared: hearts were placed in ice cold saline and cooled for 15 s and then mounted to the Langendorff apparatus (n = 5; cool immediate group); hearts were cooled for 60 s and mounted (n = 5; cool delay group); hearts were mounted directly to the apparatus within 15 s after the isolation without cooling (n = 5; noncool immediate group); hearts were mounted without cooling, but the mounting was delayed for 60 s after the isolation (n = 5; noncool delay group). All hearts were paced at a fixed rate of 300 bpm, and an occlusion of left coronary (LCA) for 60 min was performed, which was followed by reperfusion for another 60 min. Coronary flow (CBF), left ventricular developed pressure (LVDP), and creatine phosphokinase (CPK) release did not change among the four groups during ischemia. At the end of reperfusion the LVDP values were 70 +/- 1%, 66 +/- 2%, 62 +/- 3%, and 73 +/- 2% of preischemic values in cool immediate, cool delay, noncool immediate, and noncool delay groups, respectively. CPK values were 116 +/- 4, 121 +/- 7, 138 +/- 6, and 29 +/- 1 x 10(3) U/g myocardium, and percentage necrosis/risk areas were 24 +/- 1.0%, 21 +/- 1.7%, 38 +/- 2.6%, and 13 +/- 0.5% in cool immediate, cool delay, noncool immediate, and noncool delay groups, respectively. The noncool delay group demonstrated high LVDP, least amount of CPK release, and smallest size of necrosis. These results indicate that an unintentional preconditioning effect can be induced when the cooling procedure is not applied and perfusion is delayed.
authors.affiliation: First Department of Surgery Tokai University School of Medicine, Bohseidai, Kanagawa, Japan.
authors.forename: U
authors.initials: U
authors.lastname: Minhaz
authors.forename: S
authors.initials: S
authors.lastname: Koide
authors.forename: A
authors.initials: A
authors.lastname: Shohtsu
authors.forename: M
authors.initials: M
authors.lastname: Fujishima
authors.forename: H
authors.initials: H
authors.lastname: Nakazawa
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D003402:Creatine Kinase / Q000378:metabolism; D006439:Hemodynamics / Q000502:physiology; D007036:Hypothermia, Induced; D066298:In Vitro Techniques; D008297:Male; D009203:Myocardial Infarction / Q000201:enzymology / Q000209:etiology / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000150:complications / Q000201:enzymology / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000201:enzymology / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D012307:Risk Factors; D013997:Time Factors
chemical_list: D003402:Creatine Kinase