Expression of Interleukin-6 in Induced Viral Myocarditis in Mice

Viral myocarditis is considered an important cause of dilated cardiomyopathy. At preseent, two mechanisms are known to be involved in the pathogenesis of viral myocarditis and subse-quent cardiomyopathy: viral direct toxicity and immune mediated toxicity. Some authors have reported that IL-6 influences the immunologic mechanism and the virus-induced tissue damage in myocarditis. We injected encephalomyocarditis(EMC) virus to induce viral myocarditis in ICR mice. In order to study the lymphocyte subset and IL-6 expression to clarify the immune mechanism and to demonstrate the role of IL-6 in viral induced myocardial damage. The following results were obtained: 1) In virus inoculated mice, inflammation was severest at 10 days, and some serious complications developed, indicating a possible transition to dilated cardiomyopathy. 2) On analysis of the lymphocyte subset, CD4 cells were most prevalent at 5 days and CD8 cells were most prevalent at 10 and 20 days. 3) IL-6 was significantly increased and expression of IL-6 was constant, but its intensity was strongest at 5 days. In conclusion, IL-6, produced by inflammatory cells, fibroblasts, and endothelial cells, might play an important role in myocardial damage in experimentally induced EMC viral myocarditis by its direct cytotoxicity or cytokine mediated activation of cytotoxic cells.

Echocardiographic Studies on Mitral Valvular Heart Disease

Echocardiography was done with Ekoline 20 model of Smith Kline Instrument in 91 patients of mitral valvular heart disease, 46 with mitral stenosis, 10 with mitral insufficiency, 38 with mitral stenoinsufficinency and 115 normal controls. The results obtained are as follows. 1. Right ventricular dimension was 13.61+/-5.61 mm/sq m. in normal controls, 16.50+/-5.06mm/sq m. in mitral stenosis, 20.17+/-3.28mm/sq m. in mitral insufficiency, 18.61+/-8.48mm/sq m. in mitral stenoinsufficiency revealing significant increment in all mitral valvular disease groups but there was no significant difference btw. each disease groups. 2. Left ventricular end-diastolic dimensions was 29.83+/-7.06mm/sq m. in normal controls, 41.57+/-7.77mm/sq m. in mitral insufficinency, 38.48+/-10.22mm/sq m. in mitral stenoinsufficiency revealing significant increment but there was no significant difference btw. mitral stenosis and normal controls. 3. Left atrial dimension was 17.57+/-4.96mm/sq m. in normal controls, 33.22+/-5.32mm/sq m. in mitral stenosis, 35.96+/-7.35mm/sq m. in mitral insufficiency, 35.00+/-8.22 in mitral stenoinsufficiency revealing significnat increment in whole mitral valvular disease. 4. E-F slope was 90.76+/-30.20mm/sec in normal controls 18.08+/-10.3mm/sec in mitral stenosis, 29.52+/-19.3mm/sec in mitral stenoinsufficiency revealing marked decrement. In mitral insufficiency, it was 65.3+/-45.4mm/sec revealing significant decrement but not so severe as previous. 5. There was no significant difference between normal controls and mitral valvular disease in valve excursion. 6. Left atrial dimension to aortic root size was 1.13+/-0.31 in normal controls, 1.77+/-0.63 in mitral stenosis, 1.56+/-0.60 in mitral regurgitation and 1.82+/-0.56 in mitral stenoinsufficinecy revealing significant increment in whole mitral valvular heart disease.