RESUMO
Genetic control of PQ prolongation of the electrocardiogram (ECG) in the mouse, immunized with killed group A streptococci, was studied by using various congenic mice. Mice of H-2a, H-2k and H-2f haplotypes showed high frequencies of PQ prolongation, while haplotypes of H-2b, H-2d and H-2s showed low frequencies of PQ prolongation. Studies using various recombinant mice revealed that at least one immune-associated (Ir) gene mapped in the left side of the I-B subregion. High responsiveness of F1 hybrids of H-2b and H-2d, as well as B10.A(5R) and B10.A(3R), suggests the existence of a complementing gene. In addition, the differences between C3H and CKB, as well as differences between C3H.SW and CWB, indicate that another Ir gene maps in the immunoglobulin heavy chain (Igh) coding loci. Repeated injections of anti-I-J or anti-I-A antisera also modified this PQ prolongation. These results suggested that both the major histocompatibility complex (MHC) and immunoglobulin (Igh) loci seem to be playing important roles in the pathogenesis of PQ prolongation.
Assuntos
Antígenos de Bactérias , Genes MHC da Classe II , Complexo Principal de Histocompatibilidade , Cardiopatia Reumática/imunologia , Streptococcus pyogenes/imunologia , Animais , Antígenos de Bactérias/imunologia , Modelos Animais de Doenças , Eletrocardiografia , Imunização , Camundongos , Camundongos Endogâmicos , Cardiopatia Reumática/genéticaRESUMO
Prolongation of P-Q interval in the anesthetized rat was observed by repeated injection of killed group A streptococci. The prolongation was clearly recognized at about the 11th week after the first injection, but afterwards P-Q interval recovered to the normal level in spite of continuous injection of killed streptococci. His bundle electrogram recorded from isolated heart revealed the prolongation of A-H interval in the treated rat. Moreover, the transmembrane action potential in the atrioventricular nodal region of treated rat was slightly deteriorated, but the action potentials in the other cardiac muscles were not changed. It was deduced from the above results that P-Q prolongation was transiently brought about by the injection of killed group A streptocci and that deterioration of muscle in the atrioventricular nodal region might take a main part in the P-Q prolongation.
