Circulation, Vol 88, 235-244, Copyright © 1993 by American Heart Association
Z Yao and GJ Gross
BACKGROUND. The main objective of the present study was to determine the
role of adenosine in the development of myocardial stunning following
multiple, brief periods of coronary artery occlusion as well as the subtype
of adenosine receptor (A1 or A2) involved. A second objective was to
determine if there was an interaction between the adenosine A1 receptor and
the ATP-dependent K channel (KATP). METHODS AND RESULTS. The effects of the
selective adenosine A1 receptor antagonist
8-cyclopentyl-1,3-dipropylxanthine (DPCPX) and agonist cyclopentyladenosine
(CPA), the selective A2 receptor agonist CGS 21680, and the KATP channel
blocker glibenclamide on myocardial stunning produced by repetitive
coronary artery occlusions were studied in barbital-anesthetized dogs.
Regional segment function was measured with sonomicrometry. Under control
conditions, six 5-minute periods of coronary occlusion interspersed with
10-minute periods of reperfusion and ultimately followed by 2 hours of
reperfusion produced regional segment dysfunction. Pretreatment with
intravenous infusion of CPA (2.0 micrograms.kg-1.min-1) improved percent
segment shortening throughout reperfusion, whereas pretreatment with DPCPX
(1.0 mg/kg i.v. bolus) significantly worsened the recovery of postischemic
contractile function. In contrast, neither DPCPX nor CPA had any effect on
the recovery of contractile function when administered before the second
coronary occlusion. Furthermore, pretreatment with CGS 21680 (0.2
micrograms.kg-1.min-1) did not affect the recovery of percent segment
shortening. In addition, pretreatment with a low dose of glibenclamide (0.1
mg/kg) had no effect on percent segment shortening by itself but completely
abolished the beneficial effect of CPA. Importantly, the effects of the
various agents on percent segment shortening were independent of difference
in systemic hemodynamics, collateral blood flow, or ischemic bed size.
CONCLUSIONS. These results suggest that stimulation of myocardial adenosine
A1 receptors, particularly when induced by the initial coronary artery
occlusion, is cardioprotective during repetitive, brief periods of coronary
artery occlusion and that these beneficial actions may be partially
mediated via a glibenclamide- sensitive mechanism, possibly opening of
myocardial KATP channels.
ARTICLES
Glibenclamide antagonizes adenosine A1 receptor-mediated cardioprotection in stunned canine myocardium
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee 53226.
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