title: Biochemical and ultrastructural evaluations of the effect of ischemic preconditioning on ischemic myocardial injury--role of the adenosine triphosphate-sensitive potassium channel.
abstract: The aim of this study was to clarify the role of the adenosine triphosphate (ATP)-sensitive potassium channel on the mechanism of ischemic preconditioning (IP). Thirty-five anesthetized dogs were divided into 5 groups: (1) Control (C), (2) IP, (3) intravenous infusion of nicorandil (Ni) prior to IP, (4) glibenclamide (G1) pretreated with IP (G1+IP), and (5) G1 pretreated with Ni (G1+Ni). All groups had 60 min ischemia followed by 60 min reperfusion, and were analyzed by biochemical and morphological procedures. At the end of the 60-min reperfusion, %segment shortening in C indicated paradoxical bulging. This value had significantly recovered in IP and Ni groups, but it was still negative in the G1+IP and G1+Ni groups. Ca++-ATPase activity of the sarcoplasmic reticulum (SR) was significantly decreased in C. In the IP and Ni groups, this activity was significantly maintained; however, in the G1+IP and G1+Ni groups it was similar to that in C. State 3 respiration of mitochondria showed similar changes in the SR. In the ultrastructural observations, severely damaged cells were not observed in the IP and Ni groups. These results indicated that an ATP-sensitive potassium channel opener enhanced the effects of IP and its blockade abolished these phenomena. It was conclude that the ATP-sensitive potassium channel may play a key role in the mechanism of IP.
authors.affiliation: Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
authors.forename: E
authors.initials: E
authors.lastname: Geshi
authors.forename: H
authors.initials: H
authors.lastname: Ishioka
authors.forename: A
authors.initials: A
authors.lastname: Nomizo
authors.forename: M
authors.initials: M
authors.lastname: Nakatani
authors.forename: T
authors.initials: T
authors.lastname: Katagiri
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D001783:Blood Flow Velocity; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D003331:Coronary Vessels / Q000502:physiology; D004285:Dogs; D004591:Electrophoresis, Polyacrylamide Gel; D005905:Glyburide / Q000494:pharmacology; D006439:Hemodynamics; D019157:Ischemic Preconditioning, Myocardial; D008929:Mitochondria, Heart / Q000201:enzymology / Q000378:metabolism; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000201:enzymology / Q000473:pathology* / Q000503:physiopathology*; D009206:Myocardium / Q000201:enzymology / Q000648:ultrastructure; D020108:Nicorandil / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology*; D012519:Sarcoplasmic Reticulum / Q000737:chemistry / Q000201:enzymology
chemical_list: D015221:Potassium Channels; D020108:Nicorandil; D000255:Adenosine Triphosphate; D000252:Calcium-Transporting ATPases; D005905:Glyburide