BIOCHEMICAL AND ULTRASTRUCTURAL EVALUATIONS OF THE EFFECT OF ISCHEMICPRECONDITIONING ON ISCHEMIC MYOCARDIAL INJURY - ROLE OF THE ADENOSINETRIPHOSPHATE-SENSITIVE POTASSIUM CHANNEL

The aim of this study was to clarify the role of the adenosine triphos phate (ATP)-sensitive potassium channel on the mechanism of ischemic p reconditioning (IP). Thirty-five anesthetized dogs were divided into 5 groups: (1) Control (C), (2) IF, (3) intravenous infusion of nicorand il (Ni) prior to IF, (4) glibenclamide (Gl) pretreated with IP (Gl+IP) , and (5) Gl pretreated with Ni (Gl+Ni). All groups had 60min ischemia followed by 60min reperfusion, and were analyzed by biochemical and m orphological procedures. At the end of the 60-min reperfusion, %segmen t shortening in C indicated paradoxical bulging. This value had signif icantly recovered in IP and Ni groups, but it was still negative in th e Gl+IP and Gl+Ni groups. Ca++-ATPase activity of the sarcoplasmic ret iculum (SR) was significantly decreased in C. In the IP and Ni groups, this activity was significantly maintained; however, in the Gl+IP and Gl+Ni groups it was similar to that in C, State 3 respiration of mito chondria showed similar changes in the SR. In the ultrastructural obse rvations, severely damaged cells were not observed in the IP and Ni gr oups. These results indicated that an ATP sensitive potassium channel opener enhanced the effects of IP and its blockade abolished these phe nomena. It was conclude that the ATP-sensitive potassium channel may p lay a key role in the mechanism of IP.