The arachidonic acid metabolic capacity of canine myocardium is increased during healing of acute myocardial infarction.

The relative capacity for metabolizing [14C]arachidonic acid into biologically active products was studied in microsomes prepared from both normal and infarcted regions of myocardium at three different times after circumflex coronary artery occlusion in the dog. At 3 days after infarction, when polymorphonuclear leukocytes were the predominant invading cell, the ability of infarcted left ventricle microsomes to produce arachidonic acid metabolites was greater than that of microsomes from normal areas of the same hearts. At 3 weeks after infarction, when macrophages were the predominant infiltrating cell and there was a proliferation of blood vessels and fibroblasts, there continued to be significant increases in the production of both prostacyclin (measured as 6-keto PGF1 alpha) and thromboxane (measured as TxB2). This enhanced production was still seen at 3 months after infarction at a time when histological examination of the tissue showed that it was still healing with both blood vessels and fibroblasts present. The production of 6-keto PGF1 alpha was 31.7 +/- 4 picomoles per milligram protein per hour (pmol/mg per hr) in noninfarcted regions of left ventricle, whereas the production was significantly increased to 71.7 +/- 15 at 3 days, 64.1 +/- 10 at 3 weeks, and 67.2 +/- 15 even at 3 months after infarction. The thromboxane synthetase activity rose significantly from 30.1 +/- 5 pmol mg per hr in noninfarcted regions to 73.7 +/- 18 at 3 days, 71.2 +/- 5 at 3 weeks, and 92.4 +/- 40 at 3 months. The enhanced ability to metabolize arachidonic acid may result from the inflammatory cell invasion or fibroblast activation which accompany healing of acute infarcts.