BACKGROUND: Peroxisome proliferator-activated receptor-gamma(PPAR-γ) can restrain the inflammatory reaction of hypertrophic myocardium through restraining the expression of interleukin-6, cyclooxygenase, endothelin-1, nitricoxide synthase, matrix metalIoproteinase-9, gelatinase and adhesion molecule, etc.OBJECTIVE: To observe the influence of rosiglitazone sodium(the ligand for PPAR-γ) on inflammatory factors in rats with myocardial hypertrophy in the course of myocardial hypertrophy resulting from pressure load.DESIGN: Randomized controlled trial based on animals.SETTING: Department of Cardiovascular Surgery, Xinqiao Affiliated Hospital, the Third Military Medical University of Chinese PLA.MATERIALS: Fifty purebred male SD rats of S.P.F. Grade, whose body mass was (220±22) g.METHODS: The experiment was completed in the Institute of Battle Surgical Research, the Third Military Medical University of Chinese PLA from August 2004 to October 2005. Fifty rats were randomly divided into 5groups: control group, sham operation-normal saline group, sham operationrosiglitazone group, myocardial hypertrophy-normal saline group and myocardial hypertrophy-rosiglitazone group, 10 rats per group. The rat model of myocardial hypertrophy induced by pressure overload was established with the method of coarctation of abdominal aorta. Rosiglitazone group: At the postoperative 4th week, the rats were injected intraperitoneally with the Normal saline group: At the postoperative 4th week, the rats were injected intraperitoneally with normal saline[1 mL/(kg.d)] for 1 week. At the postoperative 5th week, the indexes of myocardial hypertrophy and hemodynamics were determined. The contents of tumor necrosis factor-α, platelet activating factor and myeloperoxidase in the left ventricle muscle were determined with radioimmunosorbent technique. The expression of PPAR-γ mRNA was detected with RT-polymerase chain reaction. The activity of nuclear factor-κB was detected with EMSA.MAIN OUTCOME MEASURES: The indexes of hemodynamics, cardiac ventricle reconstitution and cardiac muscle in the rat models.RESULTS: Except 1 rat in the control group died of the external injury induced by biting after 3 weeks, 49 of 50 rats entered the result analysis.①After the coarctation of aorta, the contents of tumor necrosis factor-α, platelet activating factor and myeloperoxidase of hypertrophic myocardium in the myocardial hypertrophy-rosiglitazone group were lower significantly than those in the myocardial hypertrophy-normal saline group(P ＜ 0.01-0.05), but they were still higher than those in the control group(P＜0.01).②The expressions of PPAR-γ mRNA of myocardial tissue in both the myocardial hypertrophy-rosiglitazone and myocardial hypertrophy-normal saline groups were higher obviously than those in the control group(P＜0.01), and those in the myocardial hypertrophy-rosiglitazone group were higher than those in the myocardial hypertrophy-normal saline group(P＜0.01).③The activity of nuclear factor-κB combined with DNA in cardiac muscle cell in both the myocardial hypertrophy-normal saline and myocardial hypertrophy-rosiglitazone groups were higher obviously than those in the control group (P＜0.01), and those in the myocardial hypertrophy-rosiglitazone group were lower obviously than those in the myocardial hypertrophy-normal saline group(P＜0.01).CONCLUSION: The increasing of pressure load induces myocardial hy pertrophy. The activation of nuclear factor-κB in the tissue of hypertrophic myocardium is strengthened obviously. The expressions of tumor necrosis factor-α, platelet activating factor and myeloperoxidase in hypertrophic myocardium increase. This inflammatory reaction, which is strengthened obviously, can be restrained by rosiglitazone sodium that is the synthetical lig and for PPAR-γ.

Objective To investigate the effects of rosiglitazone, an synthetic ligand of peroxisome proliferator activated receptor-?(PPAR-?) on the expression of proinflammatory factors in rats of myocardial hypertrophy. Methods The rat model of hypertrophy were established by coarctation of abdominal aorta in male SD rats, and the rats with myocardial hypertrophy were treated with rosiglitazone or physiological saline (n=10 for each therapy). Some rats underwent sham operation and were given rosiglitazone or physiological saline (n=10 for each therapy). Rosiglitazone at the dose of 4 mg?kg -1?d -1 or saline of 1 ml?kg -1?d -1 was given intraperitoneally for 1 week after postoperative 4 weeks. Another 9 rats served as control. Hemodynamics, ventricular hypertrophic index, TNF-?, PAF, MPD, PPAR-? and NF-?B were detected in all rats at postoperative 5 week. Results Significant hypertrophy was found in the left ventricle in rats undergoing the coarctation of abdominal aorta. The myocardium level of TNF-?, PAF, MPD was higher in rats with myocardial hypertrophy than in rats undergoing sham operation at postoperative 5 weeks (P

Objective To study the effects and mechanisms of growth hormone(GH) pretreatment on the inflammatory response of liver in rats after cardiopulmonary bypass(CPB).Methods The CPB model in rat was established.The rats were randomly divided into GH pretreatment group(GH group),CPB group,and sham group.The serum levels of endotoxin,TNF-?,and liver function were determined at different intervals respectively.Simultaneously,the liver tissues were collected for the detection of the CD14 mRNA and TNF-? mRNA by RT-PCR.Results Compared with pre-CPB,the serum levels of endotoxin,TNF-? were significantly increased,and the lesion of liver function was apparent in GH group and CPB group.Meanwhile,the expression of CD14 mRNA and TNF-? mRNA in liver tissues were also increased obviously in both groups.However,the serum levels of endotoxin and TNF-? and the expression of CD14 mRNA and TNF-? mRNA in liver tissues at the same time point in GH group were significantly lower than those in CPB group(P

0.05).Platelet aggregation was decreased on the 2nd postoperative day and significantly increased on the 4th postoperative day (P

Objective To investigate the role of cell apoptosis in the gut mucosal barrier dysfunction in rats undergoing cardiopulmonary bypass(CPB) . Methods The rat model of CPB was set up. The rats were divided into CPB group, sham operation(SO) group and normal control group. The morphological changes of ileum mucosal tissues were observed by microscope and electron microscope at 3h, 6h, 12h and 24h after operation, respectively. The apoptotic index of gut mucosal epithelial cells was measured with TUNEL method. Results Gut mucosal morphology was normal in CPB group at 3h, 6h and 12h after operation, but gut mucosal epithelial desquamation occurred at 24h after operation. Typical apoptotic cells could be seen with electron microscope in CPB group at every time point. Apoptotic index of gut mucosal epithelial cells significantly increased in CPB group at every time point compared with SO group, and peaked at 6h after operation. Apoptotic cells were mostly located in the gut crypt. Conclusion The data suggested that the apoptosis of intestinal epithelial cells significantly increased at early stage of post-CPB in rats, which might contribute to gut mucosal barrier dysfunction.

AIM: To investigate the effect of chronic atrial fibrillation (AF) on free calcium concentration and expression of Ca 2+ /calmodulin dependent protein kinase Ⅱ (CaMKⅡ) in human atrial myocytes. METHODS: The intracellular free calcium concentration in acute isolated atrial myocytes and the expression of CaMKⅡ in atrial tissue of rheumatic heart disease patients with atrial fibrillation (AF) and with normal sinus rhythm were measured by laser scanning cofocal microscopy technique and Western blotting, respectively. RESULTS: The intracellular Ca 2+ concentration in patients with atrial fibrillation was significantly higher than that in patients with normal sinus rhythm [(276.38?38.12) nmol/L vs (122.28?45.63) nmol/L, P

Objective To evaluate the effects of selected decontamination of the digestive tract(SDD) on intestinal derived endotoxmia,inflammation mediator and clinical outcome in patients of rheumatic heart disease undergoing valve replacement operation with cardiopulmonary bypass(CPB).Methods Thirty patients with CPB were randomly divided into control group(n=15) and treatment group(SDD group,n=15).The patients in control group routinely took preoperative preparation while those in treatment group orally administrated Tobramycin 100 mg,garlicin 40 mg and Lactulose 10ml three times per day in addition to routinely preoperative bowel preparation.The levels of endotoxin,D-lactate,TNF-? and complement 3 were measured at four time points of anesthetic induction,CPB end,2 h and 24 h after CPB.Results The level of D-lactate in the patients of SDD group was significantly lower than that of the control group at time points of anesthetic induction and 2 h after CPB(P0.05).Conclusion The endotoxemia can be induced by CPB.The regime of SDD is an effective way of preventing endotoxemia,but it may not have effect on inflammation medium and clinical outcome.

Objective To investigate the change of intestine mucosal permeability during cardiopulmonary bypass (CPB) and its effect on gut barrier in rats model. Methods The rats model of CPB was established and samples of tissue and plasma were collected at different intervals. Plasma D-lactate and LPS concentrations were determined and gut tissue was examined microscopically. Results The plasma concentration of D-lactate and LPS increased gradually at 1h CPB, and increased markedly 1h after CPB. They recovered to normal 8h after CPB, respectively. In addition, it was noted that there was a significant positive correlation between the plasma concentrations of LPS and D-lactate (r = 0.8312, P

Objective To summarize experiences in surgical treatments of 18 patients suffered from Ebstein's anomaly with intracardiac repair and bi-directional cavopulmonary shunt from January 1999 to June 2003. Methods Of 18 patients, 10 male (55.6%) and 8 female (44.4%), mean age was (18.47?13.85) years old (range from 9 months～54 years old),and mean weight of body (36.09?19.78) kg (range from 8.5～80.0 kg). All patients were in type II of Ebstein's anomaly according to WANG (Zenwei's) classification, while 15 (83.3%) were in type B, and 3 (16.7%) in type C according to Carpentier's classification. Danielson repair of Ebstein's malformation and other intracardiac repair were performed on all patients, followed by bi-directional cavopulmonary anastomosis, on pump with heart beating. Results There was no death, and no severe heart dysfunction and refractory low cardiac output in all patients postoperatively. No reoperation for residual or recurrent tricuspid incompetence was required in all patients. At follow-up of 13 (72.2%) patients ranging from 1 to 53 months, 12 patients were in New York Heart Association ((NYHA)) class I, 1 in class II. Four were with 1 grade, 2 with 2 grades tricuspid regurgitation. The patency of bi-directional cavopulmonary anastomoses was verified by echocardiography. Conclusion Ventricular unloading added to intracardiac repair appears to be effective to improve left and right ventricular function and tricuspid valve performance in Ebstein's anomaly with moderate or massive tricuspid dysfunction and physiological right ventricular outlet tract obstruction.

Objective The present study is to investigate the effect of EPO pretreatment on TNF-? expression in cultured cardiac myocytes with H/R and to explore the possible NF-?B signal transduction mechanism. Methods The model of cultured cardiac myocytes with H/R was established and the cardiac myocytes were divided into 4 groups, including EPO group (treat with EPO 10?U/ml 24?h before H/R), EPO+PDTC group (treat with EPO 10?U/mL and PDTC 5??g/ml 24?h before H/R), PDTC group (treat with PDTC 5??g /ml 24h before H/R) and control group. Change of TNF-? gene expression before and after H/R in cardiac myocytes was detected with RT-PCR and western blot. Change of NF-?B activity before and after H/R in cardiac myocytes was assayed with EMSA. Results Before H/R, there was no significant difference in TNF-? mRNA and protein expression between the 4 groups and after H/R, TNF-? mRNA and protein expression increased significantly in the 4 groups compared to control group before H/R. After H/R, TNF-? mRNA and protein expression was lower in EPO group than in the other 3 groups. Before H/R, NF-?B activity was higher in EPO group than in the other groups. After H/R, NF-?B activity increased significantly in all the 4 groups compared to the control before H/R and NF-?B activity was lower in EPO group than in the other groups. Conclusion EPO pretreatment inhibited the upregulation of TNF-? gene expression after H/R in cardiac myocytes, which might be related to the inhibition of NF-?B activation; EPO pretreatment might inhibit the activation of NF-?B after H/R through the negative feed-back mechanism of NF-?B activation.