Healing of myocardial infarction in animal models.
The experimental models used by investigators to study myocardial infarction have been considered as to their possible application for use in studies of the healing of myocardial infarction. The information concerning healing has also been surveyed. In general, the healing of the myocardial infarct in the dog and in the rat is by connective tissue replacement of the injured tissue resulting in a scar similar to skin scars. In the healing process, there is an early increase of glycoproteins, possibly from serum, and of hyaluronic acid in the injured tissue. Much of this is part of the general reaction to injury and may not be part of the healing process. Somewhat later (about 2-3 days in the dog) the chondroitin-4-sulfate fraction begins to rise. Collagen biosynthesis increases at the same time although this relationship is not well established. Much later (after 30 days in dog) the chondroitin-4-sulfate content of the injured tissue begins to decrease. At this time the scar is well formed. Much later (as late as 171 days) the scar in the myocardium still contains elevated amounts of chondroitin-4-sulfate. The dermatan sulfate is increased and the hyaluronic acid slightly decreased as compared to undamaged myocardium. These changes are typical in maturing scars of skin.
D000818:Animals; D002809:Chondroitin Sulfates / Q000378:metabolism; D003331:Coronary Vessels / Q000502:physiology; D003871:Dermatan Sulfate / Q000378:metabolism; D004195:Disease Models, Animal; D004285:Dogs; D006025:Glycosaminoglycans / Q000378:metabolism; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D006820:Hyaluronic Acid / Q000378:metabolism; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology*; D051381:Rats; D014945:Wound Healing
D006025:Glycosaminoglycans; D003871:Dermatan Sulfate; D006820:Hyaluronic Acid; D002809:Chondroitin Sulfates