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Objective To evaluate the effects of fasudil on DCD hearts .Methods Sixteen domestic ,mixed‐breed male porcine [mean body weight (28 ± 3)kg] were randomly divide into experiment group and control group (n= 8 in each) .Experiment group :animals were sedated ,anesthetized and paralyzed .Mechanical ventilation with room air was provided .After thoroctomy ,cardiac arrest was established by bloodletting ,and then keeps at room temperature for additional 25 minutes (warm ischemia) .Hearts were perfused via the aortic root with fasudil (0 .1 mg/kg) enriched cold Stanford solution for coronary artery flushing ,rapidly excised and the aorta was cannulated .Hearts were subjected to isolated Langendorff perfusion (retrograde perfused with warm oxygenated autologous blood) afterwards ,and then underwent 20 minutes of equilibrium ,immersed in fasudil (0 .5 mg/kg) enriched cold Stan‐ford solution for 2 hours in situ cold preservation .Finally ,all the hearts were resuscitated with the warm oxygenated autologous blood perfusion .Control group :hearts from the animals experienced the same except for fasudil supplement .Left ventricular per‐formances were evaluated .Coronary blood flow ,myocardial infarction volume ,myocardial water content ,and myocardial enzyme were measured .Myocardial electron microscopic examinations were carried out as well .Results All the hearts from both groups were successfully resuscitated ,fasudil significantly decreased water content ,enzyme leakage (P< 0 .01 each versus control group) , and increased coronary blood flow (P< 0 .01 versus control group) .Left ventricular function were better preserved (P< 0 .01 each versus control group) .All hearts lacked severe necrosis as determined by tetrazolium staining ,myocardial infarction volume were decresed in experiment group (P< 0 .01 each versus control group) .Intracellular components retained various types of organelle in both group ,but still ultrastructural alterations in control group were more distinctive than in experiment group .Conclusion (1) Donor heart arrested by exsanguinations and plus 25 minutes warm ischemia ,could still be resuscitated with satisfactory result ;(2) The addition of fasudil to Stanford solution (before excise of graft ,during the cold preservation) ,might alleviate DCD heart I‐R in‐jury ,improving the effect of DCD heart preservation ,and hopefully ,might be a novel arsenal in clinical DCD heart transplantation in the future .
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Objective To investigate the effect of edaravone plus beating-heart-preservation as well as beating-heart-transplantation technique on myocardial protection in donation after cardiac death (DCD) heart transplantation.Methods Twenty-four swine (body weight 28 ± 3 kg) were divided into two groups (n =12 each),and another twelve swine were used for blood donor.( 1 ) Experimental group:cardiac arrest was induced by asphyxiation (turning off the ventilation),and then the swine were subjected to 25-min warm ischemia,and cold oxygenated blood was perfused before the harvest of donor heart.Cardiac resuscitation was initiated by the ex vivo perfusion equipment and warm oxygenated blood was reperfused.Edaravone was given before harvesting of donor heart and in the early period of reperfusion.Donor hearts were kept beating throughout preservation and transplantation period.(2) Control group:all animals were treated in the same way except for without the application of edaravone.Hemodynamic,myocardial enzymes,and water content of myocardium were observed,and uhrastructural damage of cardiomyocytes was examined.Results All recipient animals could wean from cardiopulmonary bypass successfully.Left ventricular compliance and left ventricular contractility were significantly better preserved in experiment group than in control group.Though there was no significant difference in myocardial creatase level,the myocardial edema in experimental group was milder than in control group,and myocardial ultrastructure was better preserved in experimental group.Conclusion Heart from DCD,even though experienced 25-min warm ischemia after cardiac arrest by asphyxiation,still could be resuscitated via isolated heart perfusion equipment ( i.e.,beating-heart-preservation ) successfully.Furthermore,beating-hearttransplantation is feasible technically.Edaravone,a free-radical scavenger,could alleviate asphyxiation-induced myocardial injury,and further improve post-transplantation heart function.
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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.
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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.