Objective To investigate the effect of alltrans retinoic acid (atRA) on proliferative artery disease after heart transplantation. Methods Heterotopic heart transplantation model was established by Ono model with 16 inbred healthy male Wistar rats as donors and 16 SD rats as recipients. The rats were divided into chronic rejection group and atRAtreated group by complete random design, and there were 8 rats in each group. Rats in chronic rejection group were given Cyclosporine A 10 mg/(kg·d) by subcutaneous injection after operation, and those in atRAtreated group were given Cyclosporine A 10 mg/(kg·d) in the same way and atRA 10mg/(kg·d) by gavage. The transplanted hearts of rats were taken out 60 days after the transplantation. HE stain, masson stain and Van Gieson were done to analyze the rejection of transplanted hearts, the degree of vascular stenosis and myocardial fibrosis respectively.Immunohistochemistry was used to test proliferating cell nuclear antigen (PCNA). Results The area of myocardial fibrosis in chronic rejection group was obviously larger than that in atRAtreated group（63.99%±11.91% vs.34.68%±6.34%）, and there was significant difference between two groups（t=8.377，P=0.000）. The index of vascular stenosis in chronic rejection group was higher than that in atRAtreated group（62.86±17.18 vs. 40.10±8.20）. Vascular stenosis in atRAtreated group alleviated significantly, and there was significant difference between two groups（t=3.913, P=0.006）. The PCNA positive cells in chronic rejection group were obviously more than that in atRAtreated group（60.17±17.74 vs. 33.96±8.65）, and there was significant difference between two groups（t=5.387, P≤0.001）. There was a positive correlation between the PCNA positive cell ratio and the index of vascular stenosis（r=0.854, P=0.007）. Conclusion Alltrans retinoic acid can inhibit vascular disease after heart transplantation by cell proliferative pathway.
Objective To improve the myocardial protection result, observe the effects of 11,12 epoxyeicosatrienoic acid (11,12 EET) on reperfusion arrhythmias in the isolated perfused immature rabbit hearts, which underwent long term preservation. Methods Sixteen isolated rabbit hearts were randomly assigned to two groups, 8 rabbits each group. Control group: treated with St.Thomas Ⅱ solution, experimental group: treated with St.Thomas Ⅱ solution plus 11,12 EET. By means of the Langendorff technique, these isolated rabbit hearts were arrested and stored for 16 hours with 4℃ hypothermia, and underwent 30 minutes of reperfusion(37℃). The mean times until the cessation of both electrical and mechanical activity were measured after infusion of cardioplegia. The heart rate (HR), coronary flow (CF), myocardial water content (MWC), value of creatine kinase (CK) and lactic dehydrogenase (LDH), myocardial calcium content and the arrhythmias score (AS) during the period and at the endpoint of the reperfusion were observed. Results The times until electrical and mechanical activity arrest in the experimental group were significantly shorter than those in control group ; HR, CF, MWC, CK, LDH, myocardial calcium content and AS were significantly better than those in control group. Conclusions These data suggest that 11,12 EET added to the cardioplegic solution of St.Thomas Ⅱ has lower incidence rate of reperfusion arrhythmias.
Objective To summarize the experience of surgical treatment of complete atrioventricular canal defect （CAVCD） in 94 patients. Methods Ninety-four patients with CAVCD underwent surgical therapy. CAVCD were repaired by using two-patch technique in 65 patients and using single-patch technique in 29 patients. Additional cardiovascular anomalies were corrected simultaneously. Results There were 10 hospital deaths （10.6%）, 4 patients were less than 6 month old. Four patients died of severe mitral valve regurgitation, 3 died of pulmonary hypertensive crises and 3 died of low cardiac output syndrome, cerebral complications and aerothorax separately. Follow-up was completed in 84 patients, with a duration of 3-6 months. Mild degree mitral valve regurgitation was observed in 18 patients by echocardiography, mild to middle degree mitral valve regurgitation was observed in 12 patients. Conclusions Postoperative severe mitral regurgitation and pulmonary hypertensive crises were the main cause of deaths for correction of CAVCD. Early correction of CAVCD and satisfactory reconstruction of atrioventricular valve could obtain a satisfactory result, routine evaluation with intraoperative transesophageal echocardiography could result in a low operative mortality.