Intracoronary Administration of Adenosine Triphosphate Increases Coronary Blood Flow and Attenuates the Severity of Myocardial Ischemic Injury in Dogs |
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Authors: | Masafumi Kitakaze Koichi Node Kazuo Komamura Tetsuo Minamino Hiroaki Kosaka Tsunehiko Kuzuya Masatsugu Hori |
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Affiliation: | (1) Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita;(2) Department of Physiology I, Osaka University Graduate School of Medicine, Suita, Japan |
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Abstract: | ATP generates nitric oxide (NO) via activation of P2y receptors, and is degraded to adenosine. This study was undertaken to examine whether ATP causes coronary hyperemic flow via purinoceptors-, NO- and adenosine-dependent mechanisms, and attenuates the severity of contractile and metabolic dysfunction in the ischemic myocardium. In the non-ischemic canine hearts, the infusions of ATP into the coronary artery dose-dependently increased coronary blood flow. The levels of adenosine and end-product of NO in coronary venous blood over the arterial blood also increased. This hyperemic flow was partially attenuated by either 8-sulfophenyltheophylline (8SPT) or L-nitro arginine methyl ester (L-NAME), and completely blocked by the treatment with 8SPT, L-NAME and suramin (SRM). During myocardial ischemia, exogenous ATP increased coronary blood flow, and attenuated myocardial metabolic and contractile dysfunction, which was completely blunted by the treatment with 8SPT, L-NAME and SRM. We conclude that exogenous ATP increases coronary blood flow in the non-ischemic and ischemic myocardium mainly via either NO- or adenosine-dependent mechanisms. |
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Keywords: | NO NO synthase adenosine fractional shortening lactate extraction ratio |
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