Abstract

Vitamin E (E) and selenium (Se) are important antioxidant nutrients, preventing membrane damage by lipid hydroperoxides. In a previous study on E + Se deficient rats it was shown that plasma levels of lipoproteins increase dramatically. In continuation of this study a quantitative microscopic study was undertaken to determine the behavior of myocardial interstitial tissue space (ITS) in E + Se deficient rats as compared to control rats. Four rats fed on normal laboratory chow and 8 rats fed on basal diet supplemented with adequate E + Se served as control. Eight rats were fed on E + Se deficient diet. The animals were sacrificed after 13 to 20 weeks. Qualitative microscopic study showed patchy areas of hemorrhage, edema, infiltration of macrophages and myocardial damage consisting of pyknosis and coagulation necrosis in the deficient rats. Quantitative microscopic study of the apparently normal areas of myocardium of deficient rats showed a shrinkage of ITS (21.0 +/- 1.29% vs 16.51 +/- 4.62%, alpha = 0.01), whereas the ITS of normal laboratory chow and E + Se supplemented groups were similar. The myocardial fiber diameter was unchanged. Using Starling's hypothesis regarding fluid movement across capillary walls, several mechanisms could be advanced to explain this apparently paradoxical phenomenon. We contend that the interstitial fluid of normal areas of the myocardium is either absorbed by the adjacent damaged areas, or before extravasation of the intravascular proteins and swelling of ITS, the interstitial fluid is first absorbed by the intravascular compartment, due to capillary membrane damage.

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