The protective effect of mitochondrial ATP-sensitive K+ channel opener, nicorandil, combined with Na+/Ca2+ exchange blocker KB-R7943 on myocardial ischemia-reperfusion injury in rat.
To study the protective effect of mitochondrial ATP-sensitive K(+) channel (mitoK(ATP) channel) opener, nicorandil, combined with Na(+)/Ca(2+) exchange blocker KB-R7943 on myocardial ischemia-reperfusion injury in isolated rat hearts; the isolated rat heart was perfused by modified Langendorff device, after 15-min balanced perfusion, 45-min ischemia (about left and right coronary perfusion flow reduced to 5% of the original irrigation flow), and 2-h reperfusion were performed. Forty Wistar rats were randomly divided into four groups: control group, nicorandil group, KB-R7943 group, and the combination of nicorandil and KB-R7943 group. After 45-min ischemia and then 2-h reperfusion, the myocardial infarct size was 34.31% in control group, 26.35% in nicorandil group, 28.74% in KB-R7943 group, and 19.23% in combination of nicorandil and KB-R7943 group. SOD activity in coronary perfusion fluid was the highest in the combination of nicorandil and KB-R7943 group, and MDA content was the lowest. In the combination drug group compared with the control group, myocardial ultrastructural injury was significantly reduced. The combination of nicorandil and KB-R7943 significantly reduced myocardial infarct size, significantly reduced myocardial ultrastructural damage, could increase coronary perfusion fluid SOD activity, and reduced MDA levels.
Department of Cardiology, The First Affiliated Hospital, University of China Medical, China Medical University, 155th North of Nanjing Street, Heping District, Shenyang 110001, Liaoning Province, China. JDL2001@263.net
Dalin
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Jia
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D020108:Nicorandil / Q000627:therapeutic use*; D015221:Potassium Channels / Q000819:agonists* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D019831:Sodium-Calcium Exchanger / Q000037:antagonists & inhibitors* / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D013890:Thiourea / Q000031:analogs & derivatives* / Q000627:therapeutic use
C101670:2-(2-(4-(4-nitrobenzyloxy)phenyl)ethyl)isothiourea methanesulfonate; D000889:Anti-Arrhythmia Agents; D015221:Potassium Channels; D019831:Sodium-Calcium Exchanger; C117780:mitochondrial K(ATP) channel; D020108:Nicorandil; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D013890:Thiourea