Circulation, Vol 80, 1846-1861, Copyright © 1989 by American Heart Association
G Ambrosio, HF Weisman, JA Mannisi and LC Becker
The "no-reflow" phenomenon, the occurrence of areas with very low flow in
hearts reperfused after ischemia, is thought to be largely established at
the time of reperfusion as a result of microvascular damage induced by
ischemia. In the present study we sought to determine whether additional
impairment of tissue perfusion might also occur during the course of
reperfusion. Open-chest dogs were subjected to 90 minutes of left
circumflex coronary artery occlusion and reperfused for 2 minutes (n = 7)
or 3.5 hours (n = 8). Myocardial perfusion was visualized in left
ventricular slices following in vivo injection of the fluorescent dye
thioflavin-S just before killing. The area of impaired perfusion (absent
thioflavin) averaged 9.5 +/- 3.0% of the risk region in dogs reperfused for
2 minutes, whereas it was nearly three times as large in dogs reperfused
for 3.5 hours (25.9 +/- 8.2% of the risk region, p less than 0.05). Serial
measurements of flow by microspheres during reperfusion demonstrated zones
within the postischemic myocardium that were hyperemic 2 minutes after
reperfusion, with adequate flow still present at 30 minutes, but with a
subsequent marked fall in perfusion. After 3.5 hours these areas showed
negligible flow (0.13 +/- 0.3 ml/min/g) and no thioflavin uptake. Tissue
samples showing postischemic impairment in perfusion has received virtually
no collateral flow during ischemia (less than 0.01 ml/min/g), whereas
collateral flow was significantly higher in adjacent thioflavin-positive
zones (0.04 +/- 0.01 ml/min/g in endocardial samples and 0.07 +/- 0.02
ml/min/g in samples from the midmyocardium, p less than 0.001 vs.
thioflavin-negative areas). Areas that showed late impairment of flow
invariably demonstrated contraction band necrosis, which contrasted with
the pattern of coagulation necrosis observed in areas of "true" (i.e.,
immediate) no-reflow. Intracapillary erythrocyte stasis and marked
intravascular neutrophil accumulation (to levels greater than 20-fold that
found after 2 minutes reperfusion) were typically observed in areas of
delayed impairment to flow. Obstruction to flow at the capillary level was
confirmed in additional dogs in which the heart was injected postmortem
with silicone rubber to delineate the microvascular filling pattern. Areas
of absent capillary filling were much more extensive after 3.5 hours than
after 2 minutes reperfusion. Thus, this study shows that the occurrence of
areas of markedly impaired perfusion in postischemic myocardium is related
only in part to an inability to reperfuse certain areas on reflow. A more
important factor is represented by a delayed, progressive fall in flow to
areas that initially received adequate reperfusion.(ABSTRACT TRUNCATED AT
400 WORDS)
ARTICLES
Progressive impairment of regional myocardial perfusion after initial restoration of postischemic blood flow
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
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