ABSTRACT
AIM: To investigate the relation between myocardial remodeling and the genesis of serum anti-?_3-adrenoceptor autoantibody,an animal model of heart failure(HF) was established and the biological effects of the autoantibody were observed.METHODS:(1) Healthy male Wistar rats were subjected to HF by constricting the abdominal aorta.(2) The anti-?_3-adrenoceptor autoantibody in the sera of HF rats was detected by ELISA with the synthetic peptide of the second extracellular loop of the ?_3-adrenoceptor used as the antigen.(3) IgG in the positive sera from HF rats was prepared using a MabTrap Kit(Amersham).(4) The effects of the autoantibody on the contractile response of adult(isolated) cardiomyocytes and on the beating rate of cultured neonatal rat cardiomyocytes were observed.RESULTS:(1) The positive rate of anti-?_3-adrenoceptor autoantibody of rats increased from 21.05% of pretreatment to 78.95% after heart failure(P
ABSTRACT
AIM: To clarify the role of nitric oxide(NO) in ischemic preconditioning(IP) and its effects on apoptosis. METHODS: Seventy-two male Wistar rats were divided into the following six groups:ischemia/reperfusion (IR) group,IP group,IR+L-arg group,IP+L-arg group,IR+L-NAME group and IP+L-NAME group,The following changes were measured:cardiac hemodynamic parameters,infarct size,PMNs counting myocardial MPO activity and TUNEL staining.RESULTS: ①L-arg significantly attenuated ischemia/reperfusion-induced heart injury,reduced PMNs infiltration and cardiomyocyte apoptosis.②L-NAME also significantly reduced infarct size,PMNs infiltration and cardiomyocyte apoptosis compared with IR group,however,L-NAME aggravated ischemia/reperfusions-induced cardiac functional injury.③L-arg or L-NAME did not significantly alter the protective effect of ischemic preconditioning. CONCLUSION: Increased production of endogenous NO before prolonged ischemic period can protect hearts and inhibit apoptosis.L-NAME can inhibit iNOS activity and ONOO- production in reperfusion period to protect heart.