Circulation, Vol 84, 1758-1772, Copyright © 1991 by American Heart Association
RA Kloner, F Giacomelli, KJ Alker, SL Hale, R Matthews and S Bellows
BACKGROUND. There are several clinical situations in which large epicardial
coronary arteries are deprived of blood flow, such as occurs when an
obstructing thrombus or embolus lodges within a vessel or during coronary
dissection. There is little information concerning the effect of flow
deprivation on large epicardial coronary arteries. METHODS AND RESULTS. We
studied a model in which a segment of a large epicardial coronary artery
was deprived of blood flow using both proximal and distal clamps for 3
hours followed by reperfusion. On examination by light microscopy of cross
sections of the arteries, 19 +/- 6 neutrophils were present in the intima
of ischemic/reperfused vessels, whereas only a mean of 4 +/- 3 (SEM) were
present in the intima of nonischemic vessels (p less than 0.02). On
average, there were 17 +/- 9 neutrophils just under the elastic lamina in
ischemic/reperfused vessels versus none in the nonischemic vessels (p less
than 0.05); there were 16 +/- 10 neutrophils present within the media of
ischemic/reperfused vessels, and none (p less than 0.05) in the nonischemic
vessels. Electron microscopic analysis revealed that neutrophils in the
ischemic/reperfused vessels were often "sandwiched" between the endothelial
cells and the elastic lamina. Ultrastructural abnormalities within the
myocardium also revealed damage to the microvasculature, including the
presence of neutrophils within the vessels and erythrocyte stasis. To rule
out the possibility that findings in the large epicardial arteries were due
to toxic substances from static blood within the isolated arterial segment,
a protocol was performed in which blood was removed from the isolated
segment. Again, neutrophil infiltration into the vessel was observed.
Resting mean epicardial coronary artery blood flow before coronary
occlusion was 19 +/- 3 ml/min; mean coronary blood flow 2.5 hours after
reperfusion was identical at 19 +/- 3 ml/min. Response to both
endothelial-dependent vasodilation (acetylcholine) and
endothelial-independent vasodilation (nitroglycerin) challenges was normal
early after reperfusion but was depressed late after reperfusion,
suggesting progressive vascular dysfunction and hence a form of vascular
reperfusion injury in this model. CONCLUSIONS. When large epicardial
coronary arteries are deprived of blood flow, followed by reperfusion in
this model, neutrophils migrate into the vessel wall as well as into the
microvasculature. These abnormalities are associated with reduced
endothelial-dependent and endothelial-independent coronary vasodilator
reserve.
ARTICLES
Influx of neutrophils into the walls of large epicardial coronary arteries in response to ischemia/reperfusion
Heart Institute, Hospital of the Good Samaritan, University of Southern California, Los Angeles 90017-2395.
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