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Kitakaze M, Node K, Komamura K, Minamino T, Kosaka H, Kuzuya
T, Hori M. Intracoronary administration of adenosine triphosphate
increases coronary blood flow and attenuates the severity of myocardial
ischemic injury in dogs. Cardiovasc Drugs Ther. 1999;Sep;13(5):407-414.
Department of Internal Medicine and Therapeutics, Osaka University
Graduate School of Medicine, Suita, Japan.
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(omega)-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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Abstracts