ABSTRACT
BACKGROUND:Although the nickel-titanium occluder in the treatment of congenital heart disease has a better clinical effect, arrhythmia wil be more likely to develop in late stage. OBJECTIVE:To investigate the effect of nickel-titanium wire on expression of sarcoplasmic reticulum Ca~(2+)-ATPase and ryanodine receptor of rat myocardial cels. METHODS:Thirty Sprague-Dawley rats were obtained and randomly divided into two groups: experimental and control groups. The nickel-titanium wire was implanted to the apex of heart of rats in the experimental group. Rats in the control group received no special treatment. Rat mycardial cels were harvested at the 1th, 3rdand 6th months after operation. The gene and protein expressions of sarcoplasmic reticulum Ca~(2+)-ATPase and ryanodine receptor of rat myocardial cels were detected using RT-PCR and immunohistochemistry, respectively. The inflammatory reactions were detected using hematoxylin-eosin staining. RESULTS AND CONCLUSION:After the nickel-titanium wire was implanted into the rat myocardium, inflammatory reaction was induced by inflammatory cel infiltration in the experimental group, with hyperplasia of fibrous tissue. The inflammatory reaction gradualy disappeared as the implanted time extended. No inflammatory cel infiltration was visible in the control group. There was no significant difference in the gene and protein expressions of sarcoplasmic reticulum Ca~(2+)-ATPase and ryanodine receptor of rat myocardial cels at different time points after operation between these two groups. It showed that nickel-titanium wire had no influence on the expressions of sarcoplasmic reticulum Ca~(2+)-ATPase and ryanodine receptor of rat myocardial cels. These results suggest that nickel-titanium occluder-related arrhythmia may have little relationship with abnormal protein expression of sarcoplasmic reticulum Ca~(2+)-ATPase and ryanodine receptor.
ABSTRACT
Objective To observe the influence of congenital heart disease(atrial septal defect,ASD)to intervene closure on the right structure of children(0.05 ).The complication rate of children and adults were 25.0% and 21.3% respectively,and there were no significantly difference(P >0.05),and was no serious complications.Conclusion Congenital heart disease intervention of atria septal defects can improve heart right structure,which can benefit both children and adult,there is no difference in complication rates.All of these have less serious complications,high safety,curative effect affirmation.
ABSTRACT
Objective To explore the influence of proteasome inhibitor, MG-132 (N-benz0y1oxycarbonyl(Z)-Leu-Leuleucina1) on the expressions of carboxyl terminus of the Hsc70-interacting protein (CHIP) and heat shock protein 70 (HSP70) in ischemia reperfusion (I/R) rats and investigate the underlying mechanism of myocardial protection by the inhibitor. Methods Totally 54 adult SD rats were randomly divided into 3 groups, sham group (n=6), I/R group (n=24) and treatment group (I/R+T, n=24). The later 2 groups were further equally divided into 3 subgroups according different time of reperfusion. Left anterior descending (LAD) coronary artery was ligated for 30 min and then released for 2 h or 24 h or 7 d in different subgroups. Five minutes before reperfusion, MG-132 at dose of 0.75 mg/kg was given intravenously in I/R+T group,but I/R group and sham group were given the same volume of normal saline. The levels of CHIP and HSP70 at mRNA and protein level were detected by real-time PCR and Western blotting respectively. The correlation between CHIP and HSP70 expression was analyzed. Results Compared with I/R groups, the mRNA levels of CHIP and HSP70 were significantly increased in I/R+T groups (P