Objective: To analyze the mid long term results of prosthetic valves replacement. Methods: 2?141 patients underwent prosthetic valve replacement from 1978 to 2001, and 1?681 patients were followed up by completion of 78.5%, cumulate of 8?021.1 patient years and averages of 4.77 patient years each. The data were analyzed by multi factor regression and T test. Results: 92 patients died after operation. The 5 year and 10 year survival rates were (92.3?2.2)% and (90.1?2.7)%, respectively. The main complications were thromboembolism, valve mechanical malfunction, peri prosthetic leak, hemolysis and SBE. The heart function (NYHA) was significantly improved after valve replacement. Conclusion: The mid long term results of prosthetic valve replacement are rather satisfactory with low mortality and morbidity. Subvalvular structure preservation and tricuspid annuloplasty contribute can greatly improved heart function. Satisfactory myocardial protection during CPB is the key of successful operation.

Cardiopulmonary exercise test and electrocardiogram exercise test were performed in 68 patients with suspected coronary artery disease,the diagnostic value of two tests was compared with coronary angiography results as the gold standard.The results show that the sensitivity,specificity,positive predictive value and negative predictive value of electrocardiogram exercise test for coronary heart disease were 51.28％,68.97％,68.97％ and 51.28％ respectively; those for ratio of O2 pulse peak in cardiopulmonary exercise test were 51.28％,75.86％,74.07％ and 53.66％ respectively.It suggests that the results of cardiopulmonary exercise test may have the same value as electrocardiogram exercise test in diagnosis of coronary artery disease.

Objective To observe the hemodynamic change during cardiac arrest (CA) and after restoration of spontaneous circulation (ROSC) in a porcine acute pulmonary embolism model. Methods A total of 14 inbred Beijing Landraces were used to estalish the model of CA and ROSC induced by acute pulmonary embolism through injection of thrombus followed by cardiopulmonary resuscitation and thrombolytic therapy (urokinase, 15000 U/kg, iv). Five resuscitated pigs restored spontaneous circulation. Hemodynamic changes were determined at baseline, CA, ROSC, and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h after ROSC. Results Compared with the baseline, mean arterial pressure was decreased significantly, mean pulmonary arterial pressure and right ventricular pressure were increased significantly, and the heart rate had no change during CA induced by acute pulmonary embolism. The mean arterial pressure restored normal level gradually after ROSC, but was decreased at 4 h after ROSC compared with the baseline (P<0.05). The heart rate was faster at ROSC and 0.5-2 h after ROSC than the baseline (P<0.05). The mean pulmonary arterial pressure restored the baseline level after ROSC; The right ventricular pressure were decreased at 2.5 h (26.5±11.4)mmHg and 4 h (24.8±9.3)mmHg after ROSC compared with the level during CA (46.2±13.01)mmHg (P<0.05). The systemic vascular resistance peaked at 4 h after ROSC. The pulmonary vascular resistance level at ROSC was higher than the baseline [(96.5±24.8)DS/cm5 vs. (26.5±13.4)DS/cm5, P<0.05], and was decreased at 1 h and 2 h after ROSC, but was increased at 4 h and 6 h after ROSC [(98.5±0.7)DS/cm5 and (98.0±1.4)DS/cm5]. The changes of heart function: compared with the baseline, the left ventricular function at ROSC and 1-6 h after ROSC were declined significantly (all P<0.05), and right cardiac output declined at ROSC and 4 h and 6 h after ROSC (all P<0.05), and the level of cardiac function index was dropped at 1 h and 2 h after ROSC (P<0.05). Conclusions The mean arterial pressure was declined, mean pulmonary arterial pressure, right ventricular pressure and pulmonary vascular resistance were increased, cardiac function was decreased during CA induced by acute pulmonary embolism; After ROSC, hemodynamic changes were described as compensated in the early stage (1-2 h after ROSC) and decompensated (4 h after ROSC) with time.

Objective To observe the myocardial apoptosis and the molecular mechanism of captopril inhibiting myocardial apoptosis on cardiac arrest (CA) after resuscitation in a porcine acute pulmonary embolism (APE) model. Methods In this study, 29 inbred Beijing Landrace wererandomly (random number)divided into four groups (n=5, each group): control, APE-CA, restoration of spontaneous circulation (ROSC)-captopril, and ROSC-saline. The model of CA and ROSC was induced by APE through injection of thrombus followed by cardiopulmonary resuscitation and thrombolytic therapy (urokinase, 15000 U/kg, iv). Ten of 19 pigs with CA recovered to spontaneous circulation were divided randomly into the ROSC-captopril and ROSC-saline groups. Pigs in the ROSC-captopril group were treated with captopril (22.22 mg/kg) via porcine femoral vein at 30 min after ROSC. Pigs in the ROSC-saline group were treated with equal normal saline at 30 min after ROSC. The myocardial tissues were evaluated at 6 h after ROSC. Western blot was used to evaluate the protein levels of Bax, Bcl-2, Caspase-3, phosphorylated (p)-Src and phosphorylated extracellular regulated protein kinase (p-ERK1/2). Immunohistochemistry was used to evaluate the protein expression of p-Src and p-ERK1/2. Enzyme-linked immunosorbent assay was used to detect myocardial Na+-K+-ATPase levels. Statistical analysis was performed using one-way analysis of variance and pearson correlation test. Results Compared with the control group, the protein expression of Bax (0.25±0.01, 0.53±0.01, 0.37±0.05, F=14.16, P<0.05) and Caspase-3 (0.24±0.01, 0.33±0.01, 0.34±0.06, F=7.32, P<0.05) in the APE-CA and ROSC- saline group were increased significantly, and the Bcl-2 expression was significantly decreased (0.56±0.02, 0.19±0.01, 0.37±0.10, F=6.68, P<0.05). Captopril reduced the protein levels of Caspase-3 and Bax, while stimulated the Bcl-2 expression (all P<0.05). Compared with the control group, the protein expression of p-Src and p-ERK1/2 were higher and the Na+-K+-ATPase level was decreased on CA and ROSC induced by APE (all P<0.05). Compared with the APE-CA group, the p-Src expression in the ROSC-captopril group (0.46±0.01 vs. 0.35±0.06, P<0.05) was decreased significantly. Captopril inhibited the activation of p-ERK1/2 than saline group (0.41±0.10 vs. 0.26±0.07, P<0.05), but has no effect on the Na+-K+-ATPase level. The protein expression of p-Src and p-ERK1/2 were positively correlated with the Bax, and negatively correlated with the Bcl-2 respectively. The myocardial Na+-K+-ATPase level negatively correlated with Caspase-3 protein expression. Conclusions The molecular mechanism of cardiomyocyte apoptosis on CA and ROSC induced by APE might be related to decreased Na+-K+-ATPase level and activation of p-Src and p-ERK1/2. The cardiomyocyte apoptosis were inhibited by captopril through reducing the expression of p-Src and p-ERK1/2 in myocardium.

OBJECTIVE: To investigate whether kirenol, the major pharmacologically active compound of the Chinese medicinal herb , can protect mice from dextran sulfate sodium (DSS)-induced ulcerative colitis (UC). METHODS: C57BL/6 mice with or without kirenol pretreatment were treated with DSS in drinking water for 7 days to induce UC. The symptoms of UC including weight loss, diarrhea and bloody stool were observed daily and graded using the disease activity index (DAI). Colon injury of the mice was assessed by measuring the length of the colon and HE staining of the colon tissue. The levels of inflammatory cytokines produced by the mesenteric lymph nodes (MLNs) lymphocytes were measured using enzyme-linked immunosorbent assay; the apoptosis of the lymphocytes and CD4 T cells was analyzed using flow cytometry. RESULTS: The mice receiving pretreatment with kirenol showed obviously ameliorated symptoms of UC and milder pathological changes in the colon as compared with the control mice. Kirenol treatment significantly down-regulated the secretion of IFN-γ, IL-17A, IL-6 and TNF-α by the MLNs lymphocytes and increased the apoptosis of lymphocytes, especially CD4 T cells in the DSS-treated mice. CONCLUSIONS Kirenol can protect against T cell-mediated colon injury in DSS-treated mice possibly by suppressing the secretion of inflammatory mediators and inducing apoptosis of the inflammatory lymphocytes.
Animals ; Apoptosis ; Colitis, Ulcerative ; Cytokines ; Dextran Sulfate ; Diterpenes ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes