Study Of The Mechanisms Of T Lymphocytes In Myocardial Injury And Remodeling After Acute Myocardial Infarction

Objective: To study a potential role of a T cell-mediated autoimmune response in myocardial injury and remodeling after acute myocardial infarction (AMI ).Methods: Rats were killed 6 weeks after coronary ligation. 25×106 T cells from these animals were purified from spleens, and injected into syngeneic rats(group MI-T) and rats(group Sham-T) injected T cells from non-coronary ligation rats as control. 1, 6 and 24 weeks later, these recipient rats were killed. Histopathological studies were performed and cytokines including tumor necrosis factor(TNF)-α, interleukin(IL)-1β, IL-6, IL-10 were detected-which shown myocardial inflammation. To evaluate ventricular remodeling, the mRNA expression ofα,? -myosin heavy chain(MHC), matrix metalloproteinase (MMP)-2 and tissue matrix metalloproteinase inhibitor(TIMP)-2 were measured by semi-quanitative RT-PCR and hemodynamics analysis was showed by catheter technique. And two-dimensional echocardiography was performed also.Results: Compared to the control, in group MI-T, histopathological studies appeared that lymphocytes infiltration was obvious at 1 week, light at 6 weeks; and was not clear at 24 weeks. TNF-α, IL-1β, IL-6 and IL-10 could be detected at 1 week and continuously expressed till 6 weeks. High level of MMP-2 and TIMP-2 could be measured at 1 week and 24 weeks. The level ofα-MHC decreased while ?-MHC increased at 6 and 24 weeks. By hemodynamics analysis, ventricular function was shown slightly impaired. But two-dimensional echocardiography did not reveal systolic dysfunction in two groups. In the contrary, we did not observed the inflammation and myocardial remodeling in the control group. And none of the other organs (kidney, liver, lung, or brain) had evidence of infiltration.Conclusion: This study provided that when the T cells from spleens of rats after myocardial infarction were transferred into normal syngeneic rats, myocardial inflammation and injuries were occurred. And myocardial remodeling performed in the later stage. T cell-mediated autoimmune response is one possible mechanism of myocardial remodeling after acute myocardial infarction.