Circulation, Vol 85, 659-665, Copyright © 1992 by American Heart Association
JD Thornton, GS Liu, RA Olsson and JM Downey
BACKGROUND. Recent data from this laboratory indicate that pretreatment
with adenosine can protect the heart against infarction via A1- receptors,
but because of systemic hypotension, adenosine had to be given into the
coronary circulation. METHODS AND RESULTS. In this study, we tested whether
the protection could be achieved by intravenous administration of the
A1-selective adenosine agonists N6- (phenyl-2R-isopropyl)-adenosine (PIA)
and 2-chloro-N6- cyclopentyladenosine (CCPA). Nine groups of open-chest
anesthetized rabbits were subjected to 30 minutes of regional coronary
ischemia and 3 hours of reperfusion. Infarct size was determined by
tetrazolium staining. Control hearts receiving no treatment had 38 +/- 4%
of the risk zone infarcted. Preconditioning with 5 minutes of ischemia and
10 minutes of reperfusion before ischemia limited the infarct to 8 +/- 4%.
Intravenous PIA 15 minutes before 30-minute ischemia also limited infarct
size to 6 +/- 2% at the highest dose. CCPA offered similar protection. When
the PIA was given at reperfusion, infarct size was 46 +/- 6%, indicating
that receptor activation must precede ischemia to protect. Pretreatment
with CGS 21680, a selective A2-receptor agonist, caused identical
hypotension but failed to limit infarct size (43 +/- 3%), indicating again
that the A1-receptor is involved. When rabbits pretreated with PIA were
paced at 220 beats per minutes, PIA still limited infarct size (16 +/- 4%),
indicating that protection was not the result of bradycardia. CONCLUSIONS.
These results indicate that stimulation of adenosine A1-receptors causes
the heart to become resistant to ischemia and that this protection can be
achieved with intravenous administration of A1-selective agents.
ARTICLES
Intravenous pretreatment with A1-selective adenosine analogues protects the heart against infarction
Department of Physiology, University of South Alabama, Mobile 36688.
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