作者: Joseph C. Cleveland, Jr. , Daniel R. Meldrum , Robert T. Rowland , Anirban Banerjee , Alden H. Harken
关键词: Glibenclamide 、 Ischemic preconditioning 、 Atp sensitive k channel 、 Human myocardium 、 Endocrinology 、 Adenosine receptor 、 Adenosine 、 Creatine kinase 、 Chemistry 、 Internal medicine 、 Stimulation 、 Cardiology
摘要: Abstract Evidence supports the involvement of adenosine receptor stimulation and activation K ATP channels in ischemic preconditioning human myocardium. It is unknown, however, whether protection mediated by receptors dependent upon channel heart. The purpose this study was to determine adenosine-mediated against a simulated ischemia–reperfusion injury myocardium channels. Isolated right atrial trabeculae were placed tissue baths at 37°C, oxygenated with modified Tyrode solution, field stimulated 1 Hz. Trabeculae subjected 45 min normothermic ischemia (hypoxic, substrate-free buffer pacing 3 Hz.) 60 reperfusion (I/R trabeculae). preconditioned (IPC trabeculae) or (adenosine, 125 μmol/l) for 5 (ADO prior ischemic–reperfusion injury. Inhibition glibenclamide (10 combined pretreatment (ADO+GLI alone (GLI Developed force (DF) end (mean± s.e. ) compared baseline developed force, creatine kinase (CK) activity measured. I/R showed 27±2% DF, whereas IPC ADO 50±4% 43±3% respectively. ADO+GLI 25±2% GLI 23±4% DF. Tissue CK enhanced (433±63 U/g wet myocardium, 415±28 respectively). had 196±26 277±38 reperfusion. results suggest that confer functional ischemic-reperfusion, eliminated inhibition