Myocardial Connective Tissue Metabolism in Response to Injury: HISTOLOGICAL AND CHEMICAL STUDIES OF MUCOPOLYSACCHARIDE AND COLLAGEN IN RAT HEARTS AFTER ISOPROTERENOL-INDUCED INFARCTION

Arteriosclerotic and nonarteriosclerotic rats were given isoproterenol sufficient to cause massive myocardial injury. Hearts, livers, and kidneys were taken for analysis of the connective tissues at various intervals. Mucopolysaccharide was identified as Hale-positive material digestible with testicular hyaluronidase. Hexosamine and hydroxyproline were determined by chemical means. The changes in the connective tissue following infarction were divided into two phases. The first, occurring 1 to 2 days after the induction of necrosis, was characterized by extensive edema, accumulation of hexosamine, and by histologically demonstrable mucopolysaccharide. The second phase, 3 to 7 days after infarction, was characterized by changes typical of wound healing in general, involving both mucopolysaccharide and collagen deposition in foci of myocardial scar tissue formation. The increase in hexosamine was the same in arteriosclerotic breeder animals, which required one-half the dose of isoproterenol, as in virgin animals receiving the full dose of isoproterenol. Since the dose was selected to produce relatively the same degree of necrosis in each type of animal, it was thought that the increase in hexosamine was directly related to the injury and not to the isoproterenolper se . No comparable increase in hexosamine was observed in either the liver or kidney.