Role of adenosine in the regulation of coronary blood flow in dogs
with inhibited synthesis of endothelium-derived nitric oxide.
Matsunaga, Toshiro, Ken Okumura, Ryusuke Tsunoda, Shinji Tayama,
Toshifumi Tabuchi, and Hirofumi Yasue.
Division of Cardiology, Kumamoto University School of Medicine,
Kumamoto, Japan
APStracts 2:0458H, 1995.
Endothelium-derived nitric oxide (NO) regulates coronary blood flow,
but it is unclear how NO synthesis inhibition affects myocardial
metabolism. In pentobarbital-anesthetized dogs, myocardial oxygen
metabolism, adenosine release, and lactate extraction rate (LER), and
systolic ventricular wall thickening (SWT) at baseline and during
atrial pacing were estimated before and after intracoronary NG-nitro
-L-arginine methyl ester (L-NAME) infusion. Coronary blood flow and
PO2 in the anterior interventricular vein at baseline were both
significantly decreased by L-NAME (3[angstrom]a10-4M in the coronary
blood). Coronary flow was increased during pacing, which was not
affected by L-NAME. Myocardial adenosine release remained unchanged
during pacing before L-NAME, but it was significantly increased after
L-NAME. Neither LER nor SWT changed during pacing performed before
and after L-NAME. The experiment was also performed in dogs
pretreated with 8-phenyltheophylline. After L-NAME, pacing-induced
increase in coronary flow was suppressed and both LER and SWT were
significantly decreased during pacing. In conclusion, when NO
synthesis is inhibited, adenosine release is increased in response to
the increase in myocardial oxygen demand. With this compensatory
adenosine release, coronary flow is increased and ventricular
function is unaffected.
Received 28 April 1995; accepted in final form 2 August 1995.
APS Manuscript Number H402-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95