作者: Masafumi Kitakaze , Masatsugu Hori , Toshikazu Morioka , Seiji Takashima , Tetsuo Minamino
DOI: 10.1007/978-4-431-68249-3_29
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摘要: Adenosine is recognized as an important chemical mediator for myocardial and vascular functions, which may assist cardioprotection during ischemia reperfusion. receptors can be divided into two types; A1 A2 receptors, coupled with Gi Gs proteins, respectively. Stimulations of adenosine decrease or increase adenylate cyclase activity, In ischemic hearts, the major role endogenous to relax coronary smooth muscles blood flow through receptors. The vasodilatory effects are enhanced by alpha2-adrenoceptor stimulation due sympathetic activation, H+, ATP sensitive K+ channels, all occur in hearts. cardiovascular system, vasodilation not only effect adenosine. Stimulation also attenuates both free radical generation activated leukocytes aggregation platelets. On other hand, activation beta-adrenoceptor-mediated increases contractility, Ca2+ influx myocytes, norepinephrine release from presynaptic vesicles. Any these attenuate reperfusion injury. Indeed, potentially contractile dysfunction activations Furthermore, substantially limits infarct size following sustained ischemia. Endogenous has been hypothesized essential preconditioning, generally accepted limit size. We elucidated that preconditioning 5’-nucleotidase activity release, contribute reduction Taken together, we postulate hypothesis a potential modulator attenuation