Acute hemodynamic and coronary circulatory effects of experimental autoimmune myocarditis

Myocarditis and progression to cardiomyopathy is associated with focal spas m and reperfusion of the coronary microcirculation. Experimental autoimmune myocarditis (EAM), induced with cardiomyosin peptide-specific T cells in L ewis rats, was hypothesized to cause acute hemodynamic and coronary vascula ture changes. Fifteen experimental animals (5 each at 1, 2, and 3 weeks aft er T-cell injection) and eight controls were studied using the constant pre ssure variant of the isolated heart. Coronary resistance decreased while co ronary flow increased (P < 0.05) in EAM hearts after the first week. Rate-p ressure product, +dP/dt and -dP/dt, decreased while the heart/body weight r atio increased (P < 0.05) compared with controls at 1 week but not at 2 or 3 weeks. Mean local myocardial PO2, which reflects local oxygen delivery an d consumption, and MVO2 were not different for EAM hearts. However, compare d with controls EAM myocardial PO2 varied more widely and was often beyond the usual range, suggesting the occurrence of localized hypoxic and hyperox ic areas. In summary, after the first week there was a significant decrease in coronary resistance in the EAM animals, which required higher flow to m aintain a similar perfusion pressure. These changes in coronary resistance and how along with the heterogeneity and extremes of local myocardial PO2 l evels without a significant change in MVO2 may be explained by postulating development of low-resistance, high-flow hyperoxic areas which steal flow, thus causing hypoxia in other areas.