Circulation, Vol 75, 292-298, Copyright © 1987 by American Heart Association
P Golino, PR Maroko and TE Carew
The goal of this study was to determine the effects of acute
hypercholesterolemia on the evolution of myocardial infarction in a
preparation of coronary occlusion-reperfusion. New Zealand white rabbits
were fed a 2% cholesterol-enriched diet for 3 days (plasma cholesterol 329
+/- 70 mg/dl), or maintained on the control diet (plasma cholesterol 67 +/-
12 mg/dl). Temporary (30 min) coronary artery occlusion was performed in
open-chest rabbits with a suture snare. The snare was released to permit
reperfusion. When the animals were killed 5.5 hr later, left ventricles
were cut into 3 mm slices. Infarct size was determined by planimetry of
tetrazolium-stained slices while the area at risk of infarction
(hypoperfused zone) was determined by planimetry of the "cold spots" on
autoradiograms of the slices that contained 99m Tc-labeled microspheres
that had been injected 1 min after occlusion. Infarct size, expressed as
percent of the hypoperfused zone, was 42.8 +/- 1.3% (n = 10) in the control
group and was increased by approximately 100% in cholesterol-fed animals to
83.7 +/- 2.0% (n = 10, p less than .001). To test the hypothesis that
vascular obstruction (no reflow) might account for the larger infarct size,
thioflavin S was injected immediately before the animals were killed to
demarcate perfused myocardium in three additional groups of animals:
standard chow-fed rabbits (n = 5), cholesterol-fed rabbits (n = 5), and
standard chow-fed rabbits that, in addition, received an infusion of
isoproterenol (0.1 microgram/kg/min, n = 6), an intervention believed to
increase infarct size through a mechanism not dependent on the no- reflow
phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
The effect of acute hypercholesterolemia on myocardial infarct size and the no-reflow phenomenon during coronary occlusion-reperfusion
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