BACKGROUND: The mouse model of cervical heart transplantation is an ideal medical research tool for study of transplant-induced ischemia/reperfusion injury and immunological rejection.However,technical problems have limited the widespread use of mouse cervical vascularized heart transplantation.OBJECTIVE: To improve the cervical heterotopic heart transplantation in mice using the tail-cuff technique.METHODS: Isogeneic transplantation was performed from Balb/c to BALB/c mice,and allogeneic transplantation from C57BL/6 to BALB/c mice.The right common carotid artery and the external jugular vein of the recipient were equipped with a tail cuff made from 24 G and 22 G intravenous catheter,and everted over the cuff,and then connected with the aorta and the pulonary artery of donor heart,respectively.RESULTS AND CONCLUSION: A total of 36 transplants for formal experiment,12 for isogeneic transplantation,and 24 for allogeneic transplantation,were performed with a surgical successful rate of 100%.The total surgical procedure was(49.6±7.4)minutes and total ischemic time of the grafts was(28.8±4.2)minutes.In particular,the average time for vascular everting and for the reconnection of both vessels was obviously shortened.This improved tail-cuff technique shows its superiority,and can serve as an ideal method for establishing cervical heterotopic heart transplantation model in mice.

Objective To investigate the inhibitory effect of intercellular adhesion molecule-1 antisense oligodeoxynucleotide (ICAM-1-ASO) on the rejection of cardiac xenograft as well as the expression of ICAM-1 in the xenograft.Methods BALB/C mice and Lewis rats served as donors and recipients respectively. The mouse-to-rat heterotopic heart transplantation model was established. The hearts of normal BALB/C mice were harvested as control group. The xengrafts were divided into three groups: ddH2O group, control oligodeoxynucleotide group and ICAM-1-ASO group (n=10 in each group). Each donor was injected intravenously with ddH2O, control oligodeoxynucleotide or ICAM-1-ASO 6 h before operation respectively. At 48th h after transplantation, 5 xenografts in each group were collected for histopathological examination. The expression of ICAM-1 protein and mRNA in cardiac xenografts was detected by immunohistochemical method and semiquantitative reverse transcriptase polymerase reaction method. The mean survival time (MST) in each xenograft group was recorded in terms of the other 5 transplanted grafts by palpation per 12 h.Results Faint ICAM-1 expression was observed in the control group. In ddH2O group and control oligodeoxynucleotide group, capillary endothelial cells and myocytes of the grafts strongly expressed ICAM-1 and the relative density values (ICAM-1/?-actin) were also significantly higher with extensive hyperemia, edema, hemorrhage and inflammatory cells infiltrated in both groups than those in the control group. Comparatively, in the ICAM-1-ASO group, fainter ICAM-1 expression was observed and the relative density value (ICAM-1/?-actin) was also significantly lower with pathological improvement compared with those in ddH2O group and control oligodeoxynucleotide group. The MST in ICAM-1-ASO was (66.4?2.61) h, which was significantly prolonged as compared with ddH2O group and control oligodeoxynucleotide group.Conclusion ICAM-1-ASO can sequence-dependently inhibit the ICAM-1 expression of xenografts, suppress xenograft rejection and prolong the survival time of xenografts.

Objective To study the pathological characteristics of delayed xenograft rejection and the expression of donor ICAM-1 in mouse-to-rat cardiac xenografts. Methods BALB/c mice and Lewis rats served as donors and recipients respectively. The model of mouse-to-rat heterotopic heart xenotransplantation was established. The cardiac xenografts were harvested at 12 h, 24 h, 36 h, 48 h after transplantation and at the time when no pulsations could be detected in the transplanted heart respectively. The normal BALB/c mouse hearts were harvested as control group. The grafts were col lected to receive pathological and immunohistochemical examinations as well as to detect the level of ICAM-1 mRNA in the xenografts. Quantitive measurement of ICAM-1 expression in the grafts was done by using multimedia pathology imaging analysis system. RT-PCR products of xenografts were separated by agrose gels and the densities of the bands were determined by density scanning. Results The pathologic examination of xenografts showed hyperemia, hemorrhage with inflammatory cells infiltrated at 12 h after transplantation and they became more and more serious as time went on. The pathologic examination of rejected xenografts showed widespread intravascular thrombosis, hyperemi-a, hemorrhage, coagulative necrosis with a large number of inflammatory cells infiltrated. The stained color of vascular endothelial cells and cardiac myocytes was significantly more intensive in the xeno-grafts than that of normal BALB/c mouse hearts in the control group. The relative density values (ICAM-1/?-actin) were also significantly higher in the xenografts than that of the control group. Conclusion ICAM-1 expression in the xenografts was up-regulated, which was related with the development of the delayed xenograft rejection.

Objective To compare the cardioprotective efficacy of Cariporide as an adjunct in different pH cardioplegia. Methods Sixty-four male Sprague-Dawley rat hearts were randomly divided into 8 groups (8 rats in each group): 4 control groups and 4 treated groups with Cariporide as an adjunct to cardioplegia. After control perfusion in Langendorff mode with Krebs-Henseleit bicarbonate buffer (KHB) for 30 minutes, the isolated rat hearts were infused with different pH (pH=6.2 or 7.0 or 7.4 or 7.8, respectively) cardioplegia (without or with Cariporide) for 2 minutes to produce cardiac arrest and subjected to 60 minutes of 15?C arrest. In addition, during global ischemia, cardioplegia was reinfused for 2 minutes every 30 minutes, Sixty minutes after the ischemic arrest, cardioplegia was infused as terminal cardioplegia for 2 minutes, then the hearts were reperfused with Krebs-Henseleit bicarbonate buffer for 30 minutes. The hemodynamic parameters and the level of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) of coronary venous sinus drainage were measured before ischemia and during reperfusion. Myocardial and mitochondrial ultrastructures were observed under electronmicroscope. Results Application of Cariporide as an adjunct to cardioplegia improved significantly recovery of cardiac function and decreased the level of creatine kinase-MB(CK-MB), lactate dehydrogenase (LDH) of coronary venous sinus drainage (P

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

Chronic rejection remains the leading cause of chronic allograft dysfunction and late mortality after lung transplantation. Adaptive immune system and its cellular-based rejection has been the focus in the development of obliterative bronchiolitis. Recent research has identified that humoral immunity, autoimmunity, and innate immunity also contribute to obliterative bronchiolitis. This paper presents an updated review of the immune mechanisms for obliterative bronchiolitis following lung transplantation.

Objective To investigate the effects of levocarnitine used as an ingredient of cardioplegic solution on cardiomyocyte apoptosis in patients undergoing heart valve replacement under cardiopulmonary bypass (CPB) .Methods Twenty-four NYHA grade Ⅱ or Ⅲ patients of both sexes (16 males, 8 females) aged 27-67 yrs undergoing heart valve replacement under CPB were randomly allocated into 2 groups (n = 12): levocarnitine group and control group. In levocarnitine group levocarnitine 6 g was added to 1 000 ml of 4℃ St Thomas Ⅱ cardioplegic solution, while in control group equal volume of normal saline was added instead of levocarnitine. Cardioplegic solution 15 ml?kg-1 was injected to perfuse the heart every 30 min during aortic cross-clamping. The KC1 concentration of the cardioplegic solution was reduced by half for the last injection. During CPB the naso pharyngeal temperature was maintained at 25-27℃. Cardiac index (CI) and left ventricular ejection fraction (LVEF) were measured 1 day before and 7 days after operation using heart color ultrasonography. A small piece of myocardial tissue was obtained from right atrium for assessment of apoptosis using terminal deoxynueleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) . The expression of Bax and Bcl-2 in cardiomyocytes was determined by immuno-histochemistry, and Bcl-2/Bax ratio was calculated. Results The rate of restoration of spontaneous heart beat after aortic unclamping was significantly higher in levocarnitine group than in control group (86.6% vs 47.3%) (P

Objective Retrospectively discuss the effect of deep anesthesia on the post-operative complications with CPB. Methods All of the chosen patients including anesthesia group (30 cases) and deep anesthesia (30 cases) had the heart surgery under general anesthesia and CPB with the age of (56?6.4), the time of CPB (148?23.6) minutes, Medtronic membrane oxygenator, 4:1 cold blood cardioplegia, the flo of 2.0～2.4L?min -1 ?m -2 .The relative markers: operatively, the mean artery pressure (MAP), end tip oxygen saturation (SpO_2),the mean quantity of regitine (Regitine);postoperatively, the mean base-excess (BEpost), the mean quantity of 5% sodium bicarbonate per kilogram (NaHCO_3post),oxygen index, the level of blood glucose ,the duration of mechanical ventilation and intensive care unit stay , wound healing up, and the mortality. Results With deep anesthesia, the patients had more stable hemodynamic reserve operatively and significant improvements in the balance of acid-base, the lung function, the blood sugar , the wound recovery and the mortality. Conclusion The complication of postoperation with CPB is affected by the degree of anesthetic depth, and the proper depth of anesthesia can reduce the post-operative morbidity and mortality.

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.