Objective To investigate the effects of preconditioning (PC) with stromal-derived factor 1 alpha (SDF-1) on the levels of apoptosis of bone marrow stromal cells (BMSC) treated with hypoxia plus serum deprivation, and observe the therapeutic efficacy of cellular transplant with BMSC preconditioned with SDF-1 in rats with acute myocardial infarction. Methods BMSC were cultured with the whole marrow-adherence way. RT-PCR and immunohistochemistry were used to determine the expression of CXCR4. BMSC were incubated in medium for 24 h with 10 and 100 μg/L SDF-1 respectively, then treated with hypoxia plus serum deprivation for 6 h. The levels of apoptosis were detected by flow cytometry and TUNEL method. Acute myocardial infarction (AMI) model was established in SD rats, and BMSC preconditioned or non-preconditioned with SDF-1 were transplanted into border zone around infarct area, then heart function was measured after two weeks by ultrasonography. Results BMSC exhibited the CXCR4 expression. The number of apoptotic cells was significantly reduced in SDF-1 PC group than in control group (P<0.05), and 100μg/L SDF-1 PC group had the lowest level of apoptosis. AMI model was established successfully. Two weeks after BMSC transplant, significant improvement in cardiac function was observed in 100 μg/L SDF-1 PC group as compared with the non-PC group (P<0.05). Conclusions PC with the chemokine SDF-1 suppresses the apoptosis of BMSC treated with hypoxia plus serum deprivation. SDF-1 PC is a novel approach for enhancing therapeutic efficacy of cellular transplant in rats with AML

Objective To explore the protective effects of Ulinastatin on lung transplantation. Methods Orthotopic pulmonary autograft transplantation models of 24 New Zealand rabbits were established and randomly divided into four groups: groupⅠ (control group,n=6), groupⅡ(given 6000U/kg UTI 30min before ischemia, n=6), groupⅢ(given 12000U/kg UTI 30min before ischemia, n=6), groupⅣ(given 12000U/kg UTI respectively 30min before ischemia and during reperfusion, n=6). Then blood samples were taken from left and right atrium respectively before ischemia, and 30min after reperfusion for white blood cells counting. lung tissue DMA content was measured and lung biopsy were performed respectively before ischemia and 2h after reperfusion. Results Compared with groupⅠ, in groups Ⅱ,Ⅲ and Ⅳ, the white cell ratio of right atrium/left atrium was significantly lower, the ratio of wet/dry lung tissue weight and lung tissue DMA content were lower, and the pathological lesion was less. Conclusion Ulinastatin has protective effects on rabbit lung transplantation.

Aim To investigate the effect of 3,3′,4′,5,7-pentamethylquercetin(PMQ) on angiotensin Ⅱ(AngⅡ) induced cardiac fibrosis.Methods Thirty rats were randomly assigned to the 5 groups,6 each:① control group: Saline was administrated daily via gavage for 21 days;② PMQ group: PMQ(50 mg?kg-1) was administrated daily via gavage for 21 days;③ AngⅡ group: AngⅡ(288 ?g?kg-1?d-1)was injected subcutaneously daily from the 15 th day;④ PMQ+ AngⅡ group: PMQ and AngⅡ were administrated as above;and ⑤ solvent+ AngⅡ group: Solvent and AngⅡ were administrated as above.After the rats were euthanized on the 22 nd day,the myocardial hydroxyproline content,SOD activity and MDA content were measured,and the expression of collagenⅠ,collagenⅢ,and NADPH oxidase subunits Nox2 and p47phox mRNA were determined by real time-PCR.Collagen volume fraction(CVF) Ⅰand Ⅲ were detected by immunohistochemistry,and CVFⅠ/CVFⅢ was calculated.Results PMQ reduced cardiac fibrosis in AngⅡ induced hypertension rats by decreasing the myocardial hydroxyproline content,downregulating the expression of collagenⅠand collagenⅢ mRNA,and decreasing CVFⅠ,CVFⅠ/CVFⅢ.PMQ exerted antioxidant function by increasing SOD activity and decreasing MDA content and reducing the mRNA expression of NADPH oxidase subunits Nox2 and p47phox.Conclusion PMQ could reduce cardiac fibrosis,which may result from the inhibition of the expression of NADPH oxidase.The results suggest that PMQ may represent a promising therapeutic approach for CHF treatment.

Objective To study the effects and mechanisms of Lovastatin preconditioning on cardiac myocyte apoptosis in acute ischemic and reperfused (I/R) rat hearts. Methods 24 Sprague-Dawley male rats were randomly divided into three groups: control group (C); Lovastatin group (L) treated with lovastatin 15 mg/kg once a day for two weeks; Lovastatin and L-NAME group (N) treated with the same dose of Lovastatin with L group and L-NAME 30 mg/kg once a day for two weeks. Rat heart models of I/R were established with coronary occlusion 30 mintues and reperfusion 30 mintues of the left anterior descending artery after two-week administration. Expression of Bcl-2,Bax protein and myocardium apoptosis were investigated in every group. Results There was no change in blood lipin, expression of Bax protein was increased (P

Objective To study the diagnosis and treatment of pneumonia infected by Stenotrophomonas maltophilia (Sm) after open heart surgery.Methods The infections of Sm were proved by sputum culture.The data of risk factors?clinical feature and drug susceptibility were collected.Results Pneumonia of Sm occurred in 8 patients.They were often in poor conditions,in need of continuous mechanical ventilation and other inventions, and in use of extend-spectrum antibiotics.The infections of Sm hadn't special clinical manifestations. The isolates of Sm resistant to many antibiotics were usually found with other microorganisms.Conclusion It is important to pay more attention to pneumonia of Sm and to complete microbiological examinations in time,because patients after cardiosurgery are in great risk of the infection.

The effects of stromal-derived factor 1 preconditioning (PC) on apoptosis of bone mesenchymal stem cells (BMSCs) treated with hypoxia plus serum deprivation were investigated. Bone mesenchymal stem cells were cultured with the whole marrow-adherence technique. RT-PCR and immunohistochemistry were used to detect the expression of CXCR4. BMSCs were incubated in medium for 24 h with 10 ng/mL and 100 ng/mL SDF-1 respectively, and then they were treated with hypoxia plus serum deprivation for 6 h. Apoptosis rate was determined by flow cytometry and TUNEL method. The results showed that BMSCs had CXCR4 expression. The number of apoptotic cells was significantly reduced in SDF-1 PC group as compared with the control group, and 100 ng/mL SDF-1 PC group had the lowest level of apoptosis. It was concluded that SDF-1 preconditioning suppresses the apoptosis of BMSCs treated with hypoxia plus serum deprivation.

Objectiv e Renal ischemia-reperfusion ( I/R) may cause myocardial injury and dexmedetomidine ( DEX) is a new alpha-2 adrenergic agonist with the effects of antisympathia , seda-tion, and analgesia.This study was to investigate the effect of DEX on the myocardial tissue of rats at different time points after renal I/R. Methods Forty male Wistar rats were randomized into 5 groups of equal number,sham operation, 60 min renal ischemia and 3 h reperfusion (I/R1), 120 min ischemia and 3 h reperfusion (I/R2 ), 60 min ischemia and DEX+3 h reperfusion (D1), 120 min ischemia and DEX+3 h reperfusion ( D2) .Renal I/R was induced by removal of the right kidney and ligation of the left re-nal artery and vein followed by 3 hours of reperfusion.Meanwhile, intraperitoneal injection of DEX at 50μg/kg was given to the ani-mals in groups D1 and D2 at 60 at 120 min respectively after ischemia.After 3 hours of reperfusion, blood samples were collected for measurement of the concentrations of serum creatinine (Cr) and blood urea nitrogen (BUN), and renal and myocardial tissues harvested for observation of pathological changes under the light microscope and determination of the expressions of TNF-αand IL-10 by ELISA.Results Significant increases were observed in the concentrations of serum Cr and BUN , the expressions of TNF-αand IL-10 in the renal tissues and those in the myocardial tissues in groups I /R1([84.67 ±9.62] μmol/L, [8.55 ±1.08] mmol /L), I/R2 ([167.11 ±18.81] μmol/L, [13.42 ±1.25] mmol/L), D1 ([69.67 ±9.52] μmol/L, [7.56 ±0.70] mmol/L), and D2 ([114.29 ±12.50] μmol/L, [10.27 ±0.78] mmol/L), as compared with the sham operation group ([53.20 ±9.21] μmol/L, [3.75 ±0.78] mmol/L), (all P <0.05).Significant decreases was observed in the sham operation group as compared with other groups in the expressions of TNF-αand IL-10 (P<0.05).Significant decreases was observed in the D1 and D2 groups compared with other groups in the expressions of TNF-α, but increasing in IL-10.②Injury was reduced in the D1 and D2 groups compared with other groups.③The horizontal stripes of myocardial tissue disappeared in I/R1 and I/R2 decreases of inflammatory cells was observed in D1 and D2 groups compared with others. Conclusion Dexmedetomidine can attenuate myocar-dial injury induced by renal ischemia-reperfusion in rats and its inhibitory effect on inflammatory factors may be involved in the mechanism.

The mechanisms of rHu-EPO attenuating the apoptosis after myocardial infarction in rats were studied. Thirty-two rats were divided into three groups: sham operation group (Sham), acute myocardial infarction group (MI) and rHu-EPO-treated group (MI+ EPO). Acute myocardial infarction model was made by ligating the anterior descending coronary artery. rHu-EPO was administered i. p. in MI+EPO group at the dose of 5 000 IU/kg body weight immediately after the ligation. Each rat in MI+EPO group received the same dose of rHu-EPO daily the next 6 days. On the 14th day all rats underwent hemodynamic measurements and then killed. The samples were examined with HE stain, immunohistochemistry technique (bcl-2, bax) and TUNEL dyeing. The results showed that hemodynamic function in MI+ EPO group was much better than in MI group. The number of the cells positive for bax and TUNEL in MI+ EPO group was less than that in MI group. The number of the cells positive for bcl-2 in MI+ EPO group was more than that in MI group. These findings suggested that rHu-EPO could treat myocardial infarction by preventing apoptosis and attenuating post-infarction deterioration in hemodynamic function.

Objective To compare the results of mitral valve reconstruction and replacement as treatments for moderate to severe ischemic mitral regurgitation(IMR), and report the mid-term outcome. Methods From June 2002 to May 2008, 83 pa-tients with moderate IMR(35 cases) and severe IMR (48 cases) underwent coronary artery bypass grafting(CABG) combined with mitral valvuloplasty (MVP) (n = 43) or mitral valve replacement (MVR) (n = 40). There were 49 males and 34 females with a mean age of (59.3±7.5) years(51 -77years). The procedures of MVP included annuloplasty with a Dacron or autologous per-icardium ring in 21cases, commissural annuloplasty in 9, quadrangular resection of the posterior leaflet in 9 and using St. Jude mitral annuloplasty ring in 4. In the cases underwent MVR, 28 patients received mechanical prostheses and 12 received biopros-theses. Results 30-day mortality rate was 2.3% for MVP and 5.0% for MVR (P >0.05). The 30-day complication rate was similar for the 2 groups but mechanical ventilation time was longer for MVR patients. Mild MR ocurred in 6 patients with MVP (P <0.05). Sevonty-six patients were followed by outpatient department visit or telephone for (20.2 ± 4.9) months (3 - 60 months). During the follow-up period, 7 patients with MVP had mild insufficiency but free off etber complications. All the valve prothesis functioned well. However, 3 cases had thromboembolic complications and 7 late deaths were recorded in MVR group. Five-year complication-free survival rate was 90% for MVP group and 61% for MVR. Conclusion MVP resulted in excellent durability and provided significant mid-term survival benefit over MVR. MVP should be the first choice for patients with chronic IMR.

Objective Renal ischemia-reperfusion may cause myocardial injury and dexmedetomidine ( DEX)is a new alpha-2 adrenergic agonist which has the effects of antisympathia , sedation and analgesia.The article was to observe the effects of different doses of dexmedetomidine on myocardial injury induced by renal ischemia -reperfusion(I/R) in Rats. Methods 40 male Wistar rats were randomized into 5 groups(n=8 each)using a random number table: sham operation group(isolation of bilateral renal pedicles without ligation), I/R group (3 hours′reperfusion 120 minutes after the right nephrectomy and the ligation of left renal artery ), DEX low dose group, DEX middle dose group and DEX high dose group (DEX 25, 50, 100 μg/kg were respectively injected intraperitone-ally in rats of the three groups plus 3 hours′reperfusion after 120 minutes′ischemia ) .Blood samples were collected at 3 hours′reper-fusion to determine serum creatinine(Cr) and blood urea nitrogen(BUN) concentrations.Kidney and myocardial specimens were ex-tracted for microscopic examination and IL-10,TNF-αcontent were detected by ELISA. Results In sham operation group, renal structure was normal.In I/R group, a great amount of erythrocyte infiltration and interstitial infiltrating inflammatory cells were found in glomerulus and a lot of exfoliative cells were found in renal tubules .In DEX low dose group , erythrocyte infiltration and interstitial infiltrating inflammatory cells were found in glomerulus and a few exfoliative cells were found in renal tubules .In DEX middle dose group, erythrocyte infiltration and interstitial infiltrating inflammatory cells were found in partial glomerulus and a few exfoliative cells were found in renal tubules .In DEX high dose group , erythrocyte infiltration and interstitial infiltrating inflammatory cells in partial glomerulus were found and rare exfoliative cells were found in renal tubules .In sham operation group , cardiomyocytes were arranged in perfect order and normal structure , and chromatins and cytoplasms were in uniform distribution .In I/R group, edema and spongiform were obvious in cardiomyocytes , and focal coagulative necrosis was observed along with a great amount of infiltrating inflammatory cells and rare flaky bleeding .In DEX low dose group , edema and spongiform were found in cardiomyocytes , and focal coagulative necrosis was observed along with a great amount of infiltrating inflammatory cells and rare flaky bleeding .In DEX middle dose group , edema was found in cardiomyocytes , and mini focal coagulative necrosis was observed along with a small amount of infiltrating inflammatory cells.In DEX high dose group , edema was found in cardiomyocytes along with a small amount of infiltrating inflammatory cells .Com-pared with sham operation group , Cr, BUN concentrations in serum and IL-10,TNF-αcontents in kidney tissue and myocardium signif-icantly increased in I/R group, low dose group, middle dose group and high dose group(P<0.05).Compared with I/R group, IL-10 contents kidney tissue and myocardium significantly increased in small dose group (P<0.05).Cr ([167.11 ±18.81, 135.46 ± 9.80, 114.29 ±12.50, 100.15 ±8.81]μmol/L), BUN ([13.42 ±1.25, 11.73 ±1.15, 10.27 ±0.78, 9.28 ±0.52] mmol/L) concentrations in serum and TNF-αcontents in kidney tissue ([578.45 ±30.59, 530.76 ±20.59, 482.23 ±27.12, 423.14 ± 21.16]ng/L) and myocardium ([565.00 ±37.66, 517.82 ±36.89, 469.99 ±32.43, 407.41 ±23.77] ng/L) significantly de-creased in a dose-dependent manner in low , middle and high groups (P<0.05).Microscopic examination showed that the pathological changes of both kidney tissue and myocardium were significantly attenuated in low , middle and high dose group . Conclusion Dexmedetomidine can allenuate myocardial tissue injury induced by renal ischemia -reperfusion in a dose-dependent manner in rats and its mechanism may be involved with the inhibition of inflammatory factors .