QRS voltages are transiently increased at the superacute stage of experimental myocarditis.
ABSTRACT There are few reports on the precise electrocardiographic characteristics of acute myocarditis. The present study was focused on QRS voltage changes at the superacute stage of murine myocarditis.
Serial electrocardiograms were recorded during the acute stage of viral myocarditis in mice, and then the cardiac pathology was examined. After recording baseline electrocardiograms, mice (n=235) were inoculated intraperitoneally with the encephalomyocarditis virus, resulting in severe myocarditis. Electrocardiograms were serially recorded until nine days after virus inoculation (superacute stage, days 3 to 6; acute stage, days 7 to 9). Changes in heart rate and QRS voltages were analyzed.
Serial electrocardiograms revealed that heart rates began to increase after day 3, and that the sum of the QRS voltages increased on day 3 and then decreased on days 7 to 9. Trivial mononuclear cell infiltrations and interstitial edema were most frequently found in mice at the superacute stage.
Transient increase of the QRS voltages at the superacute stage of myocarditis was demonstrated, which may be due to an increase in ventricular mass caused by interstitial edema at this stage.
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ABSTRACT: The role of p53, a pro-apoptotic protein, in experimental autoimmune encephalomyelitis (EAE) was investigated using p53-deficient C57BL/6J mice. p53-deficient mice immunised with myelin oligodendrocyte glycoprotein (MOG) exhibited a more severe clinical course of EAE with more severe inflammation in the central nervous system (CNS) compared to wild-type littermates. While T and B cell responses of p53-deficient mice to MOG were comparable to those of wild-type littermates, significantly higher production of IL-6, granulocyte macrophage colony-stimulating factor and IL-10 was observed in lymphocytes exposed to MOG from p53-deficient mice than those from wild-type littermates. Furthermore, a flow cytometric analysis of Annexin V staining showed that apoptosis of CNS-infiltrating cells was less in p53-deficient mice with EAE compared to wild-type littermates. These results suggest that p53 may be involved in the regulatory process of EAE through the control of cytokine production and/or the apoptotic elimination of inflammatory cells.Journal of Neuroimmunology 03/2003; 135(1-2):29-37. · 2.96 Impact Factor