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The Journal of Thoracic and Cardiovascular Surgery, Vol 72, 631-643, Copyright © 1976 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
M Feola, M Rovetto, R Soriano, SY Cho and L Wiener
A possible protective effect of glucocorticoids on the ischemic myocardium
was investigated in in situ dog hearts subjected to regional ischemia and
in isolated rat hearts subjected to global ischemia. In the whole-animal
preparation, the left anterior descending coronary artery (LAD) was
occluded for 3 hours, or for 2 1/2 hours followed by 30 minutes of
reperfusion. Dexamethasone phosphate was randomly administered (20 mg. per
kilogram intravenously) after 15 minutes of ischemia. Its effects were
studied on the following: (1) myocardial cell membrane integrity, using
electron microscopic examination of tissue biopsies treated with colloidal
lanthanum; (2) myocardial water content, measuring the wet/dry weight of
myocardial tissue; (3) ischemic injury, by a count of fuchsinophilic cells
at light microscopy. In isolated rat hearts, ischemia was produced by a 60
per cent reduction of coronary flow. Randomized hearts were perfused for 2
hours with dexamethasone, 15 mg. per milliliter in buffered salt solution.
Study included determination of tissue water content and coronary vascular
resistance. Lanthanum was confined to the extracellular spaces in normal
dog myocardium, but it was found all intracellularly after 3 hours of
ischemia or after reperfusion. This was associated with morphologic changes
characteristic of irreversible cell injury. In the hearts treated with
dexamethasone, lanthanum remained excluded from the cells, water content
was less (p less than 0.005), and fuchsinophilia less severe (p less than
0.005). Likewise, water content was less (p less than 0.005) and the
increase in coronary vascular resistance resulting from ischemia less
severe (p less than 0.005) in the dexamethasone-treated isolated rat
hearts. Thus dexamethasone administered in pharmacologic doses, early,
appeared to stabilize the cell membrane, limit myocardial edema, and reduce
the severity of injury, both during ischemia and upon reperfusion.
ARTICLES
Glucocorticoid protection of the myocardial cell membrane and the reduction of edema in experimental acute myocardial ischemia
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