title: Enhancement of myocardial damage and alteration of lymphocyte subsets in murine model of postpartum myocarditis.
abstract: Acute viral myocarditis is considered to be one of the pathogenetic mechanisms for postpartum cardiomyopathy. In this study we examined the severity of viral myocarditis in postpartum mice infected 24 h after delivery. Although there were no differences in survival rate between postpartum mice and nonpregnant infected mice (control), the severities of myocardial damage in the postpartum mice was significantly greater than that in control mice (area of cell infiltration; 12.9 +/- 3.8 vs. 7.3 +/- 4.0%, p < 0.05 and necrosis; 49.7 +/- 10.9 vs. 30.2 +/- 7.1%, p < 0.05), and the dilatation of left ventricle was more prominent in postpartum mice both on acute and subacute phases. These results show that myocardial damage due to viral infection is enhanced in postpartum state when infected soon after delivery. Moreover the histopathological features of the myocarditis in the subacute phase is similar to that seen with dilated cardiomyopathy. Although there was no change in T cell subsets of peripheral blood between two groups, the percentages of L3T4+ (helper/inducer) cells and asialo GM1+ (NK) cells in the heart were statistically greater in postpartum mice than in control mice (L3T4+ cells; 8.7 +/- 0.4 vs. 6.1 +/- 2.0, p < 0.05 and asialo GM1+ cells; 7.8 +/- 0.9 vs. 5.8 +/- 0.9, p < 0.05). However, this increase was obviously smaller than amount of the percentage of Lyt2+ (suppressor/inducer) cells. Thus, it is unclear whether this change of T cell subsets is associated with the development of myocarditis.
authors.affiliation: Second Department of Internal Medicine, College of Medical Care and Technology, Gunma University School of Medicine, Maebashi, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yokoyama
authors.forename: T
authors.initials: T
authors.lastname: Kanda
authors.forename: T
authors.initials: T
authors.lastname: Suzuki
authors.forename: K
authors.initials: K
authors.lastname: Murata
mesh_terms: D000818:Animals; D018188:Cardiovirus Infections / Q000473:pathology*; D004686:Encephalomyocarditis virus; D005260:Female; D007694:Killer Cells, Natural / Q000276:immunology; D051379:Mice; D008809:Mice, Inbred C3H; D009205:Myocarditis / Q000382:microbiology* / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D011247:Pregnancy; D011645:Puerperal Infection / Q000382:microbiology* / Q000473:pathology; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D013997:Time Factors