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Integration of Adenosine and Noradrenergic Pathways in Cardiac Preconditioning

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Purines and Myocardial Protection

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 181))

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Abstract

Our hypothesis that ischemic stress-induced preconditioning is mediated by A1 receptors (1) has been supported by data in rabbit (2,3), dog (4) and rats (5). This proposal is based on two facts. First, reperfusion after brief cardiac ischemia elicits catecholamine release (1,6) and induces protection against a subsequent sustained ischemic challenge. Second, norepinephrine is the only endogenous a1 adrenergic agonist in the heart. Nevertheless, it is clear that repeated cycles of brief ischemia and reperfusion (cyclic ischemic preconditioning) induce adenosine formation (7), and adenosine directly preconditions myocardium (8). In contrast, the noradrenergic preconditioning hypothesis postulates that the sympathetic system responds to periods of ischemia that may be too short to invoke major ATP catabolism. Sympathetic activity may explain myocardial protection at the level of the isolated heart, as well as at the integrated CNS level, [e.g., preconditioning of virgin myocardium (9) and cardiac protection gained by kidney occlusion (10)]. In our view, preconditioning adds a novel dimension to the sympathetic “fight or flight” response: protective cardioadaptation.

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© 1996 Kluwer Academic Publishers

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Banerjee, A., Winter, C.B., Harken, A.H. (1996). Integration of Adenosine and Noradrenergic Pathways in Cardiac Preconditioning. In: Abd-Elfattah, AS.A., Wechsler, A.S. (eds) Purines and Myocardial Protection. Developments in Cardiovascular Medicine, vol 181. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0455-5_32

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  • DOI: https://doi.org/10.1007/978-1-4613-0455-5_32

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-8056-6

  • Online ISBN: 978-1-4613-0455-5

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