Objective To compare the similarities and differences in changes of cardiac muscle structure between the rat models of chronic cor pulmonale induced by hypoxia and active immunization of M2-muscarinic receptor under light microscope and electron microscope, and to explore the dependablity of the antibody effects on cardiac architecture. Methods The 48 healthy male Wistar rats were randomly divided into 4 groups: (1) Hypoxia group: the typical model of chronic cor pulmonale was established according to XUE's method; (2) Active immunization group was immunized by M2-muscarinic receptor peptide; (3) Control group was fed in normal condition; (4) Cyclosporin A group: the hypoxia group plus cyclosporin A treatment at the same time. The antibody against M2-muscarinic receptor was detected by SA-ELISA, and the pathological exemplar of cardiac muscle was observed by light microscope and transmission electron microscope. Results (1) Antibody level of M2-muscarinic receptor; the P/N values gradually increased along with the process of experiment, and the max value in active immunization group was 5. 13. At the end of the second week, the value in hypoxia group increased to 2.08, but was still less than in active immunization group (4.66). (2) Under light microscope: in hypoxia group and active immunization group, the hearts displayed significant alterations including disorder of cardiac muscle fiber, necrosis of myocardial cells together with the infiltration of inflammatory cells. There were no differences in light microscopic findings between hypoxia and cyclosporin A group. (3) Under transmission electronic microscope examination in both active immunization group and hypoxia group, the hearts showed s1imilar significant alterations such as focal cardiac muscle fiberlysis, loss of normal muscle fiber banding pattern, mitochondrial swelling and condensation, sarcoplasmic vacuolation and deposition of dense granules in both the sarcoplasmic and muscle fiber. The contour of myocyte was irregular and plasma membranes were discontinuous in some cells. All altered myocytes were fairly widely distributed throughout the myocardium. The interstitium showed edema, deposits of flocculent serum protein, activated fibroblasts and increased amounts of collagen fibers. No obvious alterations were observed in cyclosporin A group. Conclusions The positive rate and the titer of antibody against M2-muscarinic receptor are obviously increased in the rat model of chronic cor pulmonale, which indicates that there is a relationship between the antibody against M2-muscarinic receptor and the pathogenesis of chronic cor pulmonale.

Objective To study the molecular mechanism of different sensitivities to apoptosis induced by low concentration of As2O3 in PML-RARα negative HL-60 cells and PML-RARα positive NB4 cells. Meth-ods NB4 and HL-60 cells were cultured with As2O3 for 1 to 4 days; cell proliferation were detected by MTT method; the apoptosis was detected by flow cytometry,Bcl-2,Bax and Fas mRNA were determined by RT-PCR. Results The proliferation of NB4 cells was inhibited obviously by As2O3(1.0 μmol/L)with the induction of apoptosis( P <0.05) ,which was accompanied by the down-regulation of Bcl-2 mRNA expression( P <0.05)and the ratio of Bcl-2/Bax(P <0.05), but there was no obvious variation of Bax and Fas expression( P >0.05). Inhibition of proliferation and apoptosis were not obvious in PML-RARα negative HL-60 cells induced by low concentration As2O3 ( P >0.05), and there was no obvious variation of Bcl-2, Bax, Fas mRNA expres-sion or Bcl/Bax ratio( P >0.05). Conclusion The ratio of Bcl-2/Bax is contributed to the different sensitiv-ities of PML-RARα negative HL-60 cells and positive NB4 cells induced by low concentration of As2O3.