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The Journal of Thoracic and Cardiovascular Surgery, Vol 102, 688-694, Copyright © 1991 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
K Hashimoto, PJ Pearson, HV Schaff and R Cartier
To determine the mechanism(s) responsible for decreased coronary flow after
global cardiac ischemia and reperfusion, we studied 40 isolated rabbit
hearts before and after 30 minutes of normothermic ischemic arrest and
reperfusion. In the control group (n = 10) we evaluated the time course of
recovery of coronary flow, vascular reactivity, and myocardial function. In
experimental groups A (n = 10) and B (n = 10), metabolic control of
autoregulation was assessed by plots of myocardial oxygen consumption
versus coronary flow generated by incremental increases in heart rate. The
slope and intercept of these plots suggested that autoregulation of
coronary flow was maintained after ischemia. In group B hearts (n = 10)
hyperosmolar reperfusion with mannitol decreased myocardial water by 2% (p
less than 0.01) but did not increase coronary flow. Endothelium-dependent
function was assessed in group C (n = 10) by the administration of an
endothelium-dependent vasodilator (serotonin) and a smooth muscle
vasodilator (adenosine). Coronary artery smooth muscle function was
comparable in hearts before and after ischemia. However,
endothelium-dependent increases in coronary flow to serotonin were
significantly impaired after ischemia (p less than 0.01), and this was
accompanied by a significant decrease in prostacyclin synthesis by the
endothelium (p less than 0.001). Global cardiac ischemia and reperfusion
damages coronary artery endothelium, causing increased coronary vasomotor
tone; this may be an important mechanism of decreased coronary perfusion
and subsequent myocardial injury during reflow.
ARTICLES
Endothelial cell dysfunction after ischemic arrest and reperfusion: a possible mechanism of myocardial injury during reflow
Section of Cardiovascular Surgery, Mayo Clinic, Rochester, Minn.
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