Progress of aortic root enlargement surgery / 中华胸心血管外科杂志

Aortic root enlargement or aortic annulus enlargement is one of the key strategies for managing the small aortic root or small aortic annulus. Surgeons may be conservative about the risks of this method, which has limited the application in clinical surgery. Recent large clinical studies have shown that aortic root enlargement does not increase the risk of surgery and is a safe surgical procedure. This article reviews the methods of aortic root enlargement surgery including new aortic root enlargement surgery-aortic root enlargement with replacement of the noncoronary sinus with a patch and clinical outcome, which aims to provide a guidance for clinical practice.

Research advances on the apolipoptrotein A-I mimetic peptides / 中国生化药物杂志

High density lipoprotein cholesterol ( HDL-C) has received extensive attention because of its cardiovascular protective effects.Recent studies showed that HDL could promote reverse cholesterol transport ( RCT ) , be anti-inflammatory and antioxidant, and induce angiogenesis. Apolipoptrotein A-I (apoA-I), the most abundant protein of HDL, plays a pivotal role in the HDL mediated-functional activities.Short peptides based on the amphiphilic alpha helix structure of apoA-I have been designed and aimed at imitating the function of apoA-I.The function and metabolism of these mimetic peptides depend on their amino acids component and sequence , and have been proved to exert protection in against cardiovascular disease , infection, inflammation and oxidative damage, metabolic syndrome and tumor.Clinical trials confirmed their benefits, but high cost put them out of the practical applications..

Upregulation of myeloid cell leukemia-1 potentially modulates beclin-1-dependent autophagy in ischemic stroke in rats.

BACKGROUND: The mechanisms that underlie autophagy in cerebral ischemia remain poorly defined. Myeloid cell leukemia-1 (Mcl1), an anti-apoptotic member of the Bcl-2 family of proteins, regulates the balance between autophagy and apoptosis. However, little is known regarding its expression profile and contribution to cell fate in the brain following ischemic stroke. RESULTS: In this study, we investigated the expression profile and cellular distribution of Mcl1 in brains from transient middle cerebral artery occlusion (MCAO) model rats. Brain slices from sham-operated control rats showed minimal immunoreactivity for Mcl1. Mcl1 was mainly produced in neurons. Immunoreactivity for Mcl1 increased as early as 4 hours after MCAO, peaked at 24 hours, and then declined, but still remained high, at 72 hours. Mcl1 positive cells never colocalized with either cleaved caspase-3 or terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells. Both microtubule-associated protein 1 light chain 3 (LC3) and beclin-1 were evident in ischemic brain between 4 and 72 hours after MCAO. Most cells with strong LC3 staining were also labeled with beclin-1. Beclin-1 did colocalize with caspase-3 or Mcl1. Beclin-1/caspase-3 positive cells displayed the characteristic features of apoptosis including cell shrinkage and pyknotic nuclei, whereas beclin-1/Mcl1 positive cells had normal morphology. Pretreatment with 3-methyladenine attenuated autophagy without affecting the level of Mcl1 protein. CONCLUSIONS: These findings demonstrate that the expression of Mcl1 is involved in the survival of neuronal cells. In addition, the coexpression of Mcl1 with beclin-1 may attenuate beclin-1-dependent autophagy during ischemic stroke in rats.

L-arginine inhibits pulmonary hypertension by restoring the balance between endothelial nitric oxide synthase and inducible nitric oxide synthase / 中华胸心血管外科杂志

ObjectiveTo investigate the role of iNOS in the middle and late stage of pulmonary hypertension (PH) and the effect of L-Arginine(L-Arg) on these stage.MethodsThirty healthy male SD rats were randomly divided into five groups.All rats except those in control group were injected intraperitoneally (ip) with a single dose (50 mg/kg) of MCT to induce PH.Then the L3 and L5 groups were injected ip with 500 mg/kg L-Arg daily for 3 weeks and 5weeks respectively,the M3 and M5groups received a daily ip injection of the same amount of saline as L-Arg for 3 weeks and 5 weeks respectively; the same amount of saline was injected ip daily in control group for 5 weeks.Right ventricular systolic pressure(RVSP) was measured before lungs were excised for immunohistochemistry at the end of experiments. ResultsThe expressions of iNOS and elastin in M3 and M5 were higher compared to the control group,but L-Arg partly reduced the expressions of iNOS and elastin both at 3weeks and 5 weeks post-MCT.The reduction of eNOS expression in L3 and L5 groups were lower compared to M3 and M5 groups,but the eNOS expression in L3 and L5 groups were still lower than control group.ConclusionDuring the middle and late stage of PH,the expression of eNOS was decreased.The expression of iNOS was induced,which would produce numerous NO.However,these NO had no benefit on the development of PH.L-Arg could restore the balance of eNOS and iNOS,and could inhibit the development of PH,which may provide a new clues to explore the pathogenesis and treatment of PH.

Study of prolonging graft survival of discordant cardiac xenotransplantation / 中华器官移植杂志

Objective To search the way of prolonging xenograft survival of discordant cardiac xenotransplantation.Methods All animals were divided into groups A,B,C and D receiving the following combined therapies respectively:cobra venom factor (CVF) in group A,CVF and pentoxifylline (FTX) in group B,CVF and CCS (CsA,CTX,MP)in group C,CVF,PTX and CCS in group D.The recipients were given CVF 150 μg/kg(i.P) twice daily 1,4 days before transplantation;PTX 50 mg/kg daily(i.P)1 h before transplamtation,then 25 mg/kg(i.P)in an interval of 6 h until rejection thereafter;CsA 10mg/kg(i.p) daily one day and 1 h before transplantation until rejection;CTX 40 mg/kg(i.p) one day before transplantation,then 10 mg/kg(i.P)daily 1 h before transplantation until rejection thereafter;MP 10 mg/kg(i.v)1 h before transplantation,then 1 mg/kg(i.m) daily until rejection thereafter.The expression of vascular cell adhesion molecular-1 (VCAM-1) of vascular endothelial cells (EC) in cardiac xenografts was detected by using immunohistochemical staining method.Results The mean survival time of cardiac xenografts was 57.5 h (group A),77.38 h(group B),79.13 h (group C) and 98.75 h(group D),respectively.Twenty-four h after transplantation.VCAM-1 expression in the groups B and D was not upregulated,but slightly up-regulated in group C and obvious in group A.At rejection,the up-regulation of VCAM-1 expression was mildest in group D and most obvious in group A.and VCAM-1 expression in group B was milder than that in group C (P＜0.05).Conclusions CVF combined with PTX and CCS could significantly prolong the survival time of cardiac xenograft.PTX mainly protected EC and CCS mainly inhibit inflammatory cell infiltration.Combined use of them could complement and reinforce mutually.

Endothelium-derived microparticles induce endothelial cell superoxide generation and impair endothelial function / 中国病理生理杂志

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.