Objective:To study the mechanisms of chronic injury in heart allograft with chronic rejection.Methods:A model of cardiac chronic rejection in the rat based on tolerance induced through donor specific blood transfusions was used.The subpopulation and the distribution of infiltrating cells and the expression of adhesion molecule and growth factors were studied by immunohistochemistry and Northern blot analysis in the chronic rejection model.Results:Infiltrating cells were predominantly T lymphocytes and macrophages,mostly evident in the interstitial,subendocardial and perivascular areas.Allografts were demonstrated significantly elevated number of CD45+,CD4+,CD8+,TCR+,CD45RB+ cells,macrophages(ED_1) and NK cells at both 3 and 6 months compared with normal rat hearts and isografts at 3 months.Damaged areas also were observed expression of the adhesion molecules ICAM-1,LFA-1,basic fibroblast growth factor (bFGF) and transforming growth factor(TGF-?1).Northern blot analysis of total RNA,showed 5 to 6 fold upregulation of TGF-?1 mRNA in the chronic rejection model compared with normal rat hearts.Conclusion:These results suggest that T lymphocytes and macrophages play a central role in the development on chronic rejection and the increased expression of ICAM-1,LFA-1,bFGF and TGF-?1 in this model supports the involvement of these adhesion molecules and growth factors in the development of cardiac allograft vasculopaphy.

Objective To evaluate the long-term effect after mechanical valve replacement in adult patients with small aortic root,and guide clinical practice.Methods From July 2003 to February 2005,36adult patients with small amtic root(diameter≤ 19 mm)received mechanical valve replacement,23 mm CarboMedics valve were implanted in 14 patients by using of Manougnian annulus enlargiW; technique(CM group),19 mm CarboMedics Top Hat Supra-Annular Aortic valve were implanted in 22 patients(CMSA group).All of the patients were examined for cardiac functions(CF),left ventricular end-diastolic diameter (LVDD),interventricular septal thickness(IVST),left ventricular posterior wall thickness(LVPWT),pressure gradients across aortic valve(PGav),and left ventricular fractional shortening(LVFS),calculating left ventricular ejection fraction(LVEF)before operation and 6 years after operation.Twenty healthy adults were as control group.Results Compared to the preoperation,there was no statistical difference in CMSA group in IVST[(10.37 ± 2.06)mm vs.(11.03 ± 2.45)mm]and LVPWT[(10.53 ± 2.18)mm vs.(11.24 ±degrees(P＜ 0.01 or ＜ 0.05).PGav in CM group was lower significantly than that in CMSA group after 6 years [(9.24 ±5.93)mm Hg(1 mm Hg =0.133 kPa)vs.(24.30 ± 12.50)mm Hg],the difference was statistically significant(P ＜ 0.05).The indicators in CM group were not statistically significant compared to control group,while CMSA group in IVST,LVPWT,PGav was significant difference(P ＜0.05).Conclusions The long-term effect after mechanical valve replacement is satisfied in adult patients with small aortic root,especially in left ventricular function.Line valve ring augmentation larger diameter valves implanted will help reverse the left vehicular morphology.

AIM:To investigate the mechanism of endothelium-derived microparticles(EMP)-induced endothelial dysfunction and the role of superoxide anion(O-?2) in EMP-induced endothelial dysfunction.METHODS:EMP were isolated from human umbilical vein endothelial cells stimulated with plasminogen activated inhibitor-1.(1) Cultured bovine aortic endothelial cells(BAEC) were divided into 3 groups and pretreated with nothing in group 1,EMP(1?108/L) in group 2,EMP(1?108/L) + L-nitroarginiemethylester(L-NAME,1 mmol/L) in group 3 for 30 min and A23187(5 ?mol/L) stimulated O-?2 generation was determined by superoxide dismutase(SOD)-inhibitable ferricytochrome C reduction.(2) Facialis arteries(60-150 microns) were isolated from C57BL/6 mice and divided into 4 groups.The vessels were pretreated with nothing in group 1,EMP(1?108/L) in group 2,EMP(1?108/L) + SOD(2?105 U/L) in group 3,EMP(1?108/L) + polyethylene glycolated-SOD(PEG-SOD,2?105 U/L) in group 4 for 10 min and acetylcholine(ACH)-induced vasodilation was measured.RESULTS:(1) EMP significantly increased O-?2 generation in BAEC culture,which was prevented about 50% by pretreating the BAEC with L-NAME.(2) EMP significantly impaired ACH-induced vasodilation.SOD could not restore EMP-impaired ACH-induced vasodilation and PEG-SOD showed partial restoration of vasodilation.CONCLUSION:These data indicate that at least some EMP-induced endothelial dysfunction occurs by inducing intracellular O-?2 generation.It may provide a theoretical evidences in finding a multiple treatment including removal of O-?2 in the future.