Many studies have been made of damaged heart tissue of dogs immediately following injury produced by ligation of a coronary artery. However, there have been few studies of the myocardial lesion during the healing phase following myocardial injury. Judd and Wexler (1-3) have studied the healing phase of myocardial injury produced in rats by the injection of isoproterenol. These investigations showed alterations in the glycoproteins and glycosaminoglycans of healing heart tissue analogous to those found in an experimental dermal wound healing model by White, Shetlar and Schilling (4). As studies of the healing pattern resulting from the injury produced in dogs by ligation of a coronary artery have not been made, we have recently undertaken a study of the glycosaminoglycans in the healing areas of dog heart following myocardial infarction caused by the ligation of the circumflex coronary artery.Material and methods. Myocardial damage was produced in 32 mongrel dogs weighing 10-26 kg by ligation of the left circumflex coronary artery. All animals were anesthetized with sodium pentobarbital and operated under sterile conditions. Respiration was maintained with a Harvard respirator and electrocardiographic monitoring was done throughout the procedure. Lidocaine was injected to prevent ventricular fibrillation. After recovery, the dogs were fed Purina Dog Chow and water, ad libitum, and maintained in pens sufficiently large to allow for adequate exercise. Two control dogs were subjected to the same procedure except the artery was only exposed, but not ligated; one of these dogs was sacrificed after 4 days and one after 12 days.Animals were killed at various times postoperative after anesthetization with sodium pentobarbital. The heart was removed and examined for damage. Samples of injured and uninjured tissue were minced with scissors. These samples were placed in dialysis bags with 5 ml of water and dialyzed against deionized water for 48 hr with several changes of water. The tissue samples were removed from the dialysis bags and freeze dried. Tissue samples of suitable size were digested with a papain solution by the method of Mier and Wood (5). After digestion, aliquots were taken for cellulose acetate electrophoresis using Beckman Microzone equipment. Standards containing equimolar amounts of hyaluronic acid, dermatan sulfate and chondroitin-4-sulfate were applied to each electrophoretic pattern. A zinc sulfate electrolyte (0.2 M , pH 5.1) was used for quantitative work. Chondroitin-6-sulfate and heparin sulfate were utilized with the other glycosaminoglycans for identification purposes. As the electrophoresis with the zinc sulfate electrolyte does not allow separation of chondroitin-4-sulfate from chondroitin-6-sulfate, most samples were also run with calcium acetate electrolyte (0.3 M , pH 7.25) which does allow this separation. After electrophoresis on the cellulose acetate the resulting patterns were stained with Alcian Blue (6). The electrophoretic patterns were quantitated with a Beckman Microzone Densitomete...