Experimental myocardial infarction in adjuvant arthritis rats.

We studied the influence of various inflammatory reactions on the survival rate and occurrence of arrhythmias in the acute phase of experimental myocardial infarction in conscious male Sprague--Dawley CFY rats. Chronic disseminated inflammatory disease was induced by subplantar injection of Freund complete adjuvant, while chronic local inflammatory lesion was produced by carrageenan granuloma pouch method. An acute inflammatory response in the rat paw was evoked by carrageenan. Myocardial infarction was provoked by tightening a previously implanted silk loop around the left anterior descending coronary artery 14 days after the induction of adjuvant disease, and 7 days or 4 h after the production of granuloma pouch or foot edema. Carrageenan paw swelling was induced in rats showing expressed primary and slight secondary lesions due to Freund adjuvant. Adjuvant arthritis, but not granuloma pouch or acute paw edema, protected the rat against the fatal complications of coronary ligation. This effect was characterized by a significant increase in the survival rate from 30% to 63%, and a reduction in the occurrence of various types of dysrhythmias. Carrageenan paw edema was also less expressed and of shorter duration in rats with adjuvant disease. The level of cardiolopin was considerably increased in the arthritic group, while the other phospholipids showed no change. We conclude that chronic disseminated inflammation markedly alters the reactivity of conscious rats to experimental myocardial infarction. The alterations observed may be related to an increased energy supply and/or to accumulation of some endogenous antiinflammatory substances during adjuvant arthritis.