Adenosine and preconditioning in the rat heart.
نویسندگان
چکیده
1. Introduction during ischemia; (2) rate of anaerobic glycolysis; (3) ability to recover oxidative respiration, intracellular pH The report by Cave et al. [21] was a landmark paper and ionic equilibrium; and (4) degree of diastolic contrac-which demonstrated that functional recovery protection by ture and vascular integrity at onset of reperfusion. In-ischemic preconditioning (IPC) is not mediated by adeno-creased diastolic pressures subsequent to ischemic contrac-sine in the globally ischemic rat heart. This report raised ture reduce subendocardial perfusion such that zones of several issues in the field of preconditioning. (1) It was no-reflow may occur upon reperfusion. These subendocar-enigmatic in that recent studies had demonstrated a pre-dial zones of no-reflow are a perfused heart artifact due to dominant role of adenosine-receptors in preconditioning in increased vascular resistance subsequent to global ischemia the rabbit and dog so that the inability of adenosine to and contracture. Without reflow contracture cannot be precondition in the rat implied that species differences reversed and continued ischemia results in irreversible might exist in the receptor pathways that lead to initiation cardiomyocyte injury. In perfused hearts zonal no-reflow of preconditioning. (2) Since rat cardiomyocyte metabo-precedes irreversible cardiomyocyte injury. In perfused lism preferentially relies upon exogenous glucose to hearts irreversible injury is not confined to the endocardial support glycolysis, whereas the rabbit, dog, pig and man zone, and develops only after prolonged ischemia (45 min are more dependent upon endogenous glycogen, this report coronary artery occlusion [2] or 60–90 min sustained opened the possibility that species-dependent metabolic substrate-free anoxic perfusion [3] in the rat). Reperfusion differences could also be involved in the mechanisms of following irreversible injury in both perfused hearts and IPC. (3) Since adenosine did not appear to precondition hearts in situ results in abrupt oxygen induced enzyme the rat, emphasis was placed on multiple G-protein cou-release and contraction band necrosis. In perfused hearts pled receptors that can induce preconditioning, e.g., a-mediators that improve subendocardial reflow may im
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عنوان ژورنال:
- Cardiovascular research
دوره 45 1 شماره
صفحات -
تاریخ انتشار 2000