Circulation, Vol 81, 1921-1927, Copyright © 1990 by American Heart Association
PJ Pearson, HV Schaff and PM Vanhoutte
Experiments were designed and performed to determine whether endothelial
function remained chronically impaired after coronary artery reperfusion.
Canine left anterior descending coronary arteries were exposed to ischemia
(60 minutes) followed by reperfusion (12 weeks). Rings (3-4 mm wide) of the
reperfused artery and of normal left circumflex (control) coronary artery
segments were suspended in organ chambers containing physiological saline
solution (37 degrees C, gassed with 95% O2-5% CO2) for isometric force
measurement. Endothelium- independent contractions to KCl or prostaglandin
F2 alpha and endothelium-independent relaxations to nitric oxide or
isoproterenol were comparable in control and chronically reperfused
arteries. However, chronically reperfused coronary arteries exhibited
impaired endothelium-dependent relaxations to aggregating platelets. In
addition, the reperfused coronary arteries exhibited impaired
endothelium-dependent relaxations to the platelet-derived compounds
adenosine diphosphate, serotonin, and thrombin. However, the
endothelium-dependent relaxations to acetylcholine were comparable between
control and reperfused arteries. Thus, after 12 weeks of reperfusion,
previously occluded coronary arteries exhibited a selective impairment of
endothelium-dependent relaxation evoked by aggregating platelets. In vivo,
this phenomenon could favor platelet adhesion, aggregation, and
platelet-induced contraction of coronary smooth muscle and thus facilitate
ischemic events such as vasospasm and coronary thrombosis.
ARTICLES
Long-term impairment of endothelium-dependent relaxations to aggregating platelets after reperfusion injury in canine coronary arteries
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota.
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