Abstract:Aim To investigate the association between expression and activity of matrix metalloproteinase-9(MMP-9) and type 2 diabetic macroangiopathy and explain the mechanism of anti-atherosclerosis effect of Rosiglitazone. Methods Type 2 diabetic rat model was established by high-fat diet and a low dose of STZ. The activity of MMP-9 in arterial wall was observed by SDS-PAGE zymography. The MMP-9 mRNA expression in arterial wall was observed by RT-PCR.Meanwhile the changes of MMP-9 expression and activity were observed after Rosiglitazone treatment for 4,8 and 12 weeks. Results The activity of MMP-9 in model rats was 1.27 times as high as that of control rats,with the prolongaton of diabetes duration and the development of macroangiopathy,its activity increased progressively and was 1.69,2.25 and 2.92 times of control rats,respectively,at week 4,8 and 12 after DM.MMP-9 mRNA in model rats was 1.15,1.30,1.45 and 1.99 times higher than that of control rats at week 0,4,8 and 12 after DM.MMP-9 activity was dropped by 11.56%,37.73% and 48.60% in Rosiglitazone group after treatment for 4,8 and 12 weeks.MMP-9 mRNA was dropped by 26.80%,27.16% and 46.46% in Rosiglitazone group after treatment for 4,8 and 12 weeks. Conclusions The changes of MMP-9 expression and activity occured during the development of type 2 diabetic macroangiopathy.The mechanisms of anti-atherosclerosis effect of Rosiglitazone might be related to inhibiting MMP-9 expression and activity.

Abstract:Aim To observe the effects of Xuezhikang on Ca²⁺ concentration and mitochondrial membrane potential in hepatocytes of apolipoprotein E gene-knock out mice. Methods The hepatocytes of ApoE~(-/-) mice were separated with collagenase and cultured in RPMI1640 with 10% fetal bovine serum for 8 days.Then the hepatocyes were incubated in culture medium with 10% Xuezhikang-containing rat serum for 48 hours.Finally,after stained with flou-3/AM and JC-1,the Ca²⁺ concentration and the mitochondrial membrane potential in hepatocytes were detected with laser scanning confocal microscope. Results Xuezhikang could decrease Ca²⁺ concentration in hepatocytes and there was significant difference between Xuezhikang group and control group(p<0.01).Xuezhikang could also improve mitochondrial membrane potential in hepatocytes(p<0.05). Conclusion Xuezhikang can decrease the Ca²⁺ concentration and improve mitochondrial membrane potential in hepatocytes.This may be important mechanisms of Xuezhikang in anti-hyperlipemia.

Abstract:Aim To investigate the effect of macrophage colony-stimulating factor(M-CSF) on the expression and activity of matrix metalloproteinases(MMP) in RAW264.7 cell. Methods Gelatin zymography analysis was used to detect the effect of M-CSF on activity of MMP-9 in cultured RAW264.7 cell.Reverse transcription polymerase chain reaction(RT-PCR) was used to detect the effect of M-CSF on expression of MMP-9 mRNA in cultured RAW264.7cell. Results The enzyme activity of MMP-9 was significantly increased after 24 h M-CSF treatment.M-CSF had no effect on the activation of MMP-9 secreted.RT-PCR showed that M-CSF upregulated MMP-9 mRNA expression after 8hour M-CSF treatment. Conclusion M-CSF upregulates MMP-9 expression in RAW264.7 cell,which may play an important role in plaque destabilization.

Abstract:Aim To investigate the effects of mast cells degranulation on plaque development and their possible mechanisms in animal experiments by dealing apolipoprotein E gene-knock out(apoE~(-/-)) mice which had been placed perivascular common carotid collars with mast cells degranulator-Compound 48/80. Methods 12-week-old male apoE~(-/-) mice were fed a western-type diet and operated with perivascular right common carotid collar placement.4 weeks after surgery,mice were divided into 2 groups with 20 mice each.The experimental mice were intraperitoneally injected with Compound 48/80,0.5 μg/g,every other day;the control mice received the same injection of an equal volume of D-Hank's.Thirty minutes after 4th injection,animals were sacrificed to obtain carotid sections.Sections were routinely stained with hematoxylin and eosin.Corresponding sections on separate slides were stained with toluidine blue and immunohistochemically with antibodies against a macrophage-specific antigen or α-smooth muscle actin. Results Administration of Compound 48/80 did not affect the lipid contents of mice serum.However,the percentage of degranulated mast cells(80.6% ±17.8% vs 13.5%±4.1%,p<0.01) and the activity of tryptase in serum(0.57±0.13 u/L vs 0.36±0.10 u/L,p<0.05) were significantly increased.There were no pathological changes in common carotids non-collar placement but atheromatous plaques occured in common carotids collar placement of both groups.Significant increase in plaque area of maximum cross section(58 500±7 500 μm~2 vs 8 600±2 800 μm~2,p<0.01),the degree of lumen stenosis(81%±15% vs 41%±12%,p<0.05) and the expressions of αsmooth muscle actin(1 219±364 iu vs 522±137 iu,p<0.05)and macrophage-specific antigen(426±133 iu vs 169±38 iu,p<0.05)were detected in plaque of common carotids collar placement in the experimental group. Conclusions Perivascular common carotid collar placement can accelerate atherosclerotic plaque formation in apolipoprotein E-knock out mice. Compound 48/80 increases plaque area of maximum cross section and the degree of lumen stenosis by promoting proliferation of smooth muscle cells and accumulation of macrophages.

Abstract:Aim To determine the effect of scutel laria barbata alkaloid(LCLAs)on proliferation of cultured vascular smooth muscle cell(VSMC)induced by endothelin(ET). Methods Rat aortic VSMC was cultured and divided into four groups: ET group,ET+LCLAs group,ET+BQ-123(the selective ETA receptor antagonist)group and control group,then the cell proliferation activity was subsequently quantified by cell counting kit-8 to count cell number,~3 H-TdR incorporation to measure DNA synthesis and quantitative immunohistochemical technique to investigate the expression of proliferating cell nuclear antigen(PCNA)in VSMC.Cytotoxicity was measured by Lactate Dehydrogenase(LDH)colorimetry and Trypan blue exclusion tests. Results Compared with the control group,ET-1(10~(-7)mol/ L)significantly enhanced the proliferation activity of VSMC(p<0.01),50 mg/L LCLAs inhibited the increase of cell number(6.01±0.05,p<0.05) and ~3 H-TdR incorporation(1 464±45 counts/min,p<0.05)compared with ET group,but has no evident effect on the proliferation activity of PCNA.100,200 mg/L LCLAs and 10~(-6)mol/L BQ-123 markedly decrease the cell number(5.73±0.09,4.81±0.08,4.77±0.06,respectively),~3 H-TdR incorporation(1 263±41,1 129±49,1 140±56 counts/min,respectively)and the expression of PCNA(350±29,341±53,336±39,respectively)compared with ET group(p<0.01). Conclusions LCLAs(50～200 mg/L)inhibited ET-1-induced proliferation of VSMC in a dose-dependent manner and the effect was not due to nonspecific cytotoxicity.

Abstract:Aim To investigate the effect of tissue factor pathway inhibitor(TFPI) gene transfer on the migration of vascular smooth muscle cell and the mechanism of its inhibition on the restenosis. Methods Human tissue factor pathway inhibitor recombinant adenovirus and LacZ recombinant adenovirus were used to infect rabbit aortic vascular smooth muscle cell respectively in vitro.The transfection efficiency was examined by X-gal staining.The exogenous tissue factor pathway inhibitor gene expression in transfected cell was detected by reverse transcription-polymerase chain reaction(RT-PCR) and its effect on migration was tested with slide method. Results When multiplicity of infection was 100,the transfection efficiency was 95 percent.Expression of tissue factor pathway inhibitor mRNA was detected in TFPI gene transfected vascular smooth muscle cell at 3rd day after gene transfer.At the same concentration,the migration distances were remarkably reduced in tissue factor pathway inhibitor gene transfected groups compared with the control group(p<0.001),and had a dependence of concentrations. Conclusions Adenovirus has a higher transfection efficiency on the cultured vascular smooth muscle cell.Tissue factor pathway inhibitor gene transfer mediated by adenovirus can greatly inhibit the migration of cultured rabbit vascular smooth muscle cell and have a dependence of concentration.

Abstract:Aim To study the effect of Huomai Yin on atherosclerosis. Methods The experimental model of atherosclerosis in rabbits was established by endothelial injury by balloon and hyper-lipid feed.The atheroslerosis plaque area,collagen and matrixmetalloproteinase-1 differences between groups were evaluated at the end of the study. Results At the end of 8 weeks after endothelial injury by balloon,the plaque area in Huomai Yin highdose group(every day 12 g/kg) was smaller than that in hyper lipid group(p<0.01);compared with simvastatin group,the plaque area in highdose group was larger,but the difference wasn't significant(p<0.05);compared with hyper lipid group,the plaque area in lowdose group(every day 6 g/kg) wasn't significantly smaller(p<0.05).Collagen was reduced in highdose group and lowdose group than in hyper lipid group(p<0.01,p<0.05).Collagen wasn't significantly different between highdose group and simvastatin group(p<0.05),but collagen in lowdose group was more than simvastatin group(p<0.05). The express of matrixmetalloproteinase-1 in highdose group and simvastatin group wasn't significantly different(p<0.05),but was higher than that in hyper lipid group(p<0.01). Conclusions Huomai Yin has therapeutic effect on atherosclerosis in rabbit.Huomai Yin could modulate the express of matrixmetalloproteinase-1 and decrease collagen accumulation in the atherosclerosis plaque.

Abstract:Aim To evaluate the effects of inhibition of CD40-CD40 ligand system on development of atherosclerosis and the stability of lesions. Methods Eighteen male apolipoprotein E gene knockout mice were divided into positive control group(n=10) and anti-CD40 ligand antibody group(n=8).Serum lipids,soluble vascular cell adhesion molecule-1 and soluble intercellular adhension molecule-1 were deteced.The aortas were taken for histomorphometry observation.The positive percentage of macrophage cells,smooth muscle cells and CD4~+T cells were determined by immunohistochemistry,and the expression of matrix metalloproteinase-9 were mesurated by Western blotting. Results Anti-CD40 ligand treatment could lower the levels of serum soluble vascular cell adhesion molecule-1 and soluble intercellular adhension molecule-1(p<0.01).It had no impact on serum lipids(p<0.05).Compared with positive control group,anti-CD40 ligand group showed a reduction in plaque area,plaque/intima size ratio,vascular thickness(p<0.05).Inhibition CD40-CD40 ligand also could reduce the amount of macrophage cells and CD4~+T cells,increase the amount of smooth muscle cells(p<0.05).The expression of matrix metalloproteinase-9 decreased in anti-CD40 ligand antibody group(p<0.01). Conclusions Inhibition of CD40-CD40 ligand could decrease vascular inflammation,prevent development of atherosclerosis.It had no impact on serum lipids.

Abstract:Aim To observe the role of puerarin on the proliferation of vascular smooth muscle cells(VSMC) induced by thrombin and the effect of puerarin on the Bcl-2 protein and thrombin receptor(TR) mRNA expression. Methods Cell number and cell cycle analysis using flow cytometry were adopted as two different indicators of effects on proliferation of VSMC.Western blot was used to indicate the changes of Bcl-2 protein,and reverse transcription-polymerase chain reaction(RT-PCR) was used to evaluate TR mRNA expression,with treatment of thrombin and puerarin after 24 h. Results Thrombin can significantly increase the cell numbers of VSMC,the peak of proliferation curve is at 24 h,and the effect of T is in a dose dependent manner(0.1～1.0 u/L).1.5×10~(-5)～1.5×10~(-3) mol/L puerarin can significantly suppress this stimulation of VSMC proliferation and DNA synthesis.Western blot demonstrated that treated with thrombin and puerarin after 24 h,thrombin can significantly increase Bcl-2 protein.1.5×10~(-5)～1.5×10~(-3) mol/L puerarin can significantly suppress this increase.RT-PCR demonstrated that thrombin can increase TR mRNA expression significantly,and 1.5×10~(-3) mol/L puerarin can suppress this increase. Conclusions Puerarin can suppress the proliferation and DNA synthesis of VSMC promoted by thrombin.This inhibitory effects of puerarin are closely related with the suppression of Bcl-2 protein,and partly related with the suppression on TR mRNA.

Abstract:Aim To explore phenotypic modulation of vascular smooth muscle cells(VSMC) and change of p38,mitogen-activated protein kinase phosphatase-1(MKP-1) expression after intimal injury. Methods The model of vascular restenosis established by intimal injury of rabbit carotid arteries was used.Immunohistochemistry,Western blot and reverse transcriptase-polymerase chain reaction(RT-PCR) were used to detect the changes of proliferation cell nuclear antigen(PCNA),smooth muscle α-actin(SM α-actin),p38 protein,and MKP-1 protein as well as its mRNA of sham-injured arteries and injured arteries at different time points. Results PCNA was negative in the medium and endothelium in shaminjured arteries.Positive cell rate of PCNA was gradually increased at 1～14 days in the medium and at 5～14 days in the neointima after injury,but it declined gradually after 28 days.Positive cell rate of PCNA in the neointima was slightly more than that in the medium at different time points.SM α-actin was positive in the medium,negative in the endothelium in sham-injured arteries.SM α-actin initially decreased in the medium at 1 day,it was minimal at 3 days after injury,but it increased gradually after 5 days.Positive expression of SM α-actin in the neointima was slightly lower than that in the medium.p38 was negative or feeble positive in the medium in sham-injured arteries.p38 was continuously increased at 1～35 days after injury.Positive expression of p38 in the neointima was higher than that in the medium.There was positive relationship between change of p38 and that of PCNA in the vascular wall at different time points after injury.MKP-1 was feeble positive or positive in sham-injured arteries.MKP-1 initially decreased at 1 day and increased graduallv from 14～28th day,but it was still lower than that in the sham-injured arteries on 35th day after injury.There was negative relationship between change of MKP-1 and that of PCNA in the vascular wall at different time points after injury. Conclusion There was close relationship between phenotypic modulation and proliferation ability of VSMC.p38 and MKP-1 participated in phenotypic modulation of VSMC and its regulation after intimal injury.

Abstract:Aim To study the effect of atorvastatin on the expression of cyclooxygenase-2(COX-2) and other proinflammatory molecules in a rabbit model of atherosclerosis and to further explore the potential mechanism of atorvastatin in anti-atherosclerostic inflammation beyond the lowing lipid. Methods Twenty-four male New Zealand rabbits(3 months old)were fed with normal diet(n=8) and high-cholesterol diet(n=16) respectively for 8 weeks,and then the high-cholesterol diet rabbits were assigned to receive either atorvastatin 2.5 mg/(kg·d)(n=8)or starch(n=8).6 weeks later,aortas were removed under deep anesthetization.The femoral arteries were removed to determine COX-2 mRNA by reverse transcription-polymerase chain reaction and the level of COX-2 and matrix metalloproteinase-9(MMP-9) protein by immunohistochemistry. Atherosclerotic lesions were measured by experienced pathologist under Beihang Pathology Imaging Analysis System in aortas from hypercholesterolemic rabbits.Plasma interleukin-6(IL-6) levels were measured by enzyme linked immunosorbent assay(ELISA). Results Compared with placebo-treated group,atherosclerotic area was reduced in atorvastatin-treated group(43.0%±12.5% vs 83.0%±11.6%,p<0.05).COX-2 mRNA expression in aortas from hypercholesterolemic rabbits were significantly increased compared with those from normal rabbits,and significantly reduced by the treatment of atorvastatin(1.03±0.09 vs 0.57±0.10,p<0.05),and the levels of COX-2 mRNA expression were related to both atherosclerotic area and plasma IL-6 levels(r=0.803 and 0.795,both p<0.05).Expression of COX-2 protein in atherosclerostic plaques were significantly increased and reduced by the treatment of atorvastatin(62.4%±8.5% vs 34.3%±8.8%,p<0.05),and the levels of COX-2 were related to the levels of MMP-9 in atherosclerostic plaques(r=0.815,p<0.05). Conclusion In hypercholesterolemic rabbits,atorvastatin can decrease circulating IL-6 level and MMP-9 level in plaque,and the potential mechanism of atorvastatin in anti-atherosclerostic inflammation may be through the COX2 signal pathway.

Abstract:Aim To study the effect of insulin-like growth factor-1 receptor antibody on vascular smooth muscle cell proliferation. Methods Seven days after balloon injury,rat's carotid arteries were harvested,smooth muscle cell were cultured in vitro and were evaluated by α-actin immunocytochemical method.The effects of insulin-like growth factor-1 receptor antibody on smooth muscle cell proliferation were observed by BrdU immunocytochemical methods. Results Smooth muscle cell derived from injured arteries shows higher proliferetion compared with those from normal arteries(p<0.01),insulin-like growth factor-1 receptor antibody monoclonal antibody can inhibit smooth muscle cell proliferation concentration dependently(p<0.01). Conclusion Insulin-like growth factor-1 receptor antibody can inhibit smooth muscle cell proliferation,which deserves to be researched deeply.

Abstract:Aim To investigate the effects of static magnetic field on proliferation,ultra-microstructure,apoptosis of human umbilical vascular endothelial cells. Methods The effects of static magnetics on proliferation of human umbilical vascular endothelial cells was observed by MTT;transmission electric microscopy was used to evaluate the ultra-microstructure of human umbilical vascular endothelial cells;apoptosis of human umbilical vascular endothelial cells was studied by flow cytometry and transmission electric microscopy. Results 0.05 mT magnetics can accelerate the proliferation of human umbilical vascular endothelial cells;0.1 mT magnetics have no effects on the growth of human umbilical vascular endothelial cells,however,magnetics of 1 mT,5 mT attenuate growth of human umbilical vascular endothelial cells.5 mT static magnetics could induce apoptosis and necrosis of human umbilical vascular endothelial cells. Conclusion The effects of static magnetics on human umbilical vascular endothelial cells is double edge-sword,5 mT static magnetic field does harm to human umbilical vascular endothelial cells.

Abstract:Aim To investigate the role of sex hormone in development of CHD by assessing the serum level of estrogen,testosterone,the ratio of E₂/T and their relation with serum lipids in female member of myocardial infarction(MI) pedigrees. Methods Female members from eligible MI pedigrees were selected,and divided into two groups,coronary group: 21 members who suffered CHD,health group: 22 healthy members in MI pedigrees.Control group was consisted of 22 healthy volunteers from non CHD pedigrees.Serum estrogen,testosterone,and serum lipids were assayed. Results There is no difference about age,blood pressure among three groups.The level of serum estrogen of CHD members was almost as same as that of health group and control group,but the serum testosterone in coronary group was much higher than that in health group and control group.There is no difference between the latter two groups. Especially,the ratio of E₂/T in coronary group was significant lower,compared with the healthy group.Additionally,the ratio of E₂/T was positively related to HDLC,while negatively related to TC,TG,LDLC. Conclusion In MI pedigrees,the development of CHD in female members has no relation with the level of endogenous estrogen,while the level of endogenous testosterone especially the ratio of E₂/T seems to play an important role during this event through influencing the lipid metabolism.

Abstract:Aim To investigate the expression of interleukin-2(IL-2),interleukin-8(IL-8) and their relations with cerebral water content in rats following intralcerebral hemorrhage. Methods The rats were infused with autologous fresh blood taken from rat femoral artery into the right caudate nucleus IL-2 and IL-8 in the perihematoma and were determined with radioimmnoassay method over a time course ranging from 6 hours to 10 days.The brain water content was measured by dry-wet weight method. Result Compared with those in the control group,the levels of IL-2 in the perihematoma within 1 day after intracerebral hemorrhage(ICH) were significantly lower,slightly lower at 3-day point and highest at 6-day point,then gradually decreased;the levels of IL-8 in the perihematoma within 6 hours after ICH were not significantly different,highest in 1-day point and 3-day point,and gradually reduced to the normal level at 6-day point;the contents of edema in the perihematoma within 1 day slightly reduced,were highest at 3-day point,then gradually decreased and reached the normal levels at 6 days. Conclusion IL-2 may benefit to decrease the formation and development of brain edema, accelerate the extinction of brain edema and facilitate the recovery of nervous system function;there was immunoreaction conducted by IL-8 which led to damage after ICH,and IL-8 may be related to the produce and development of brain edema.

Abstract:Aim To study the characteristic of liver X receptor(LXR)α and its target gene expression and cholesterol efflux from human macrophages of coronary atherosclerotic disease. Methods Human monocyte-derived macrophages from coronary atherosclerotic disease(CAD) patients and controls was collected.Before being detected apolipoprotein A_Ⅰ-mediated human monocyte-derived macrophage cholesterol efflux and LXRα and mRNA expression of its target gene,the macrophages was induced with or without TO-901317. Results Compared with control normal macrophage,the mRNA levels of LXRα and its target gene expression was changed,and the macrophage cholesterol efflux was decreased.After LXR activated,the reactive capacity was also decreased from human monocyte-derived macrophage of CAD patients. Conclusions The changed function of cholesterol efflux and some gene expression may be the pathogenetic cause,and macrophage LXR activity may offer potential therapeutic benefit in the treatment of CAD.

Abstract:Aim To study the Changes of serum soluble intercellular adhesion molecule-1(sICAM-1) and its relations with endothelial dysfunction in type 2 diabetes mellitus patients. Methods 62 cases of type 2 diabetes were divided into three groups: complication free group(n=19),microangiopathy group(n=20) and macroangiopathy group(n=23).20 normal subjects were served as normal control group(n=20).Levels of sICAM-1 and von Willebrand factor(vWF) were measured by enzyme linked immunosorbent assay(ELISA). Results The levels of sICAM-1 and vWF in type 2 diabetes mellitus were higher than those in healthy controls(p<(0.01)).The levels of sICAM-1 and vWF in type 2 diabetic patients with microangiopathy were higher than those without vascular complication(p<(0.01)),but lower than those with macroangiopathy(p<(0.01)).The levels of vWF in type 2 diabetic patients without vascular complication were not higher than those in healthy controls (p<0.05).There was a significant positive correlation between sICAM-1 and vWF,triglyceride and diastolic blood pressure(r=0.43,r=0.45, r=0.52 and r=0.62,p<0.01). Conclusions Serum sICAM-1 might participate in the course of diabetic microangiopathy.The measurement of serum sICAM-1 levels in type 2 diabetes mellitus may be clinically useful for early discovering of endothelial dysfunction.

Abstract:Aim To evaluate pregnancy-associated plasma protein A(PAPP-A) as an early sensitive and specific marker indicating the instability of atherosclerotic plaques in patients with acute coronary syndromes(ACS). Methods In 20 patients with acute myocardial infarction(AMI),25 with unstable angina pectoris(UAP), 21 with stable angina pectoris(SAP),and 15 controls without coronary heart disease,the levels of PAPP-A were measured.Meanwhile,C-reactive protein(CRP),Interlukin-6(IL-6),the MB isoenzyme of creatine kinase(CK-MB) and cardian troponin Ⅰ(cTnⅠ) were examined. Results The PAPP-A,CRP and IL-6 levels were significantly higher in patients with AMI and UAP than in patients with SAP and controls(p<0.01).In patients with ACS(including AMI aand UAP),PAPP-A correlated with levels of CRP and IL-6,but not with markers of myocardial injury CK-MB and cTnⅠ. Conclusions PAPP-A levels are elevated in ACS.These increased levels may reflect the instability of atherosclerotic plaques in coronary artery,not representing specific mocardial necrosis.

Abstract:Aim To explore the effect of lipid disorders on the expression and activation of complement. Methods 41 patients with dyslipidemia were distributed into hyperlipemic group(HLP) and hyperlipemia combined with vascular diseases group(HLPC) according to clinical complications.HLP included 17 subjects with dyslipidemia,HLPC included 24 subjects suffered from dyslipidemia combined with cardiovascular diseases,cerebral vascular or peripheral vascular diseases,17 healthy subjects with similar age and gender served as controls.The serum complement components C3,C4,properdin,the plasma complement terminal complex(sC5b-9)and inflammatory markers tumor necrosis factor α(TNF-α),interleukin 6(IL-6) were examined. Results The concentration of C3 was higher in HLP(1.57±0.41 g/L)and HLPC(1.60±0.40 g/L)than in the control group(1.30±0.27 g/L)(both p<0.05);the properdin level was increased in HLP compared with control group(0.46±0.08 g/L vs 0.38±0.07 g/L)(p<0.01).The concentration of sC5b-9 in HLPC(298±110 mg/L)was increased than in HLP(233±101 mg/L)and control group(228±84 mg/L)(both p<0.05).The concentration of TNF-α was also elevated in HLPC than in HLP and controls, there is a significant increase of IL-6 in HLP and HLPC compared with controls.Univariate analysis showed serum C3,C4,Pf were positively correlated with TC,TG,LDLC,HDLC(except Pf with TG),sC5b-9 was positively correlated with SBP,DBP and TNF-α,but no correlation was found between sC5b-9 and lipids. Conclusions The complement components were significantly increased in serum of patients with dyslipidemia,which were positively correlated with lipidemic indexes. No correlation was found between sC5b-9 and lipids,but sC5b-9 was increased in patients with cardiovascular diseases.

Abstract:Aim To study effects of acute normovolemic hemodilution(ANH) on hemodynamics,hemorheology,oxgen transport and consumption during Ileat-Golon Bladder Replacement Operation on coronary heart disease patierts. Methods Thirty-eight coronary heart disease patients(28 males,10 females) aged 41～63 years weighing 47～75 kg undergoing elective Ileat-Golon Bladder Replacement Operations were randomly divided into 2 groups with 19 patients in each group: ANH group and control group.Right internal jugular vein was cannulated with 7F Swan-Ganz floating cannula for central venous pressure(CVP) monitoring and blood sampling radial artery was cannulated blood pressure monitoring and blood gas analysis,femoral vein was cannulatel for blood sampling and fluid infusion.Blood(8～12 mL/kg) was removed from radial artery in ANH group and normovolemic was maintained by simultaneous infusion of 6% HEAS.Electrocardiogram(ECG),blood pressure(BP),central venous pressure were continuously monitored throughout the operation.Arterial and central venous blood samples were taken for blood gas analysis before and after ANH. Results There were no significant changes in heart rate(HR),mean arterial pressure(MAP),mean pulmonary artery pressure(MPAP),pulmonary capillary wedge pressure(PCWP) and CVP after ANH.There were no significant difference in parameters of blood gas analysis between two groups. Conclusion ANH can be safely used for coronary heart disease during Ileat-Golon Bladder Replacement Operations,and acute normovolemic hemodilution may have heart protection function.

Abstract:Aim To explore the relationship between metabolic syndrome(MS)and arterial stiffness. Methods According to the international diabetes federation(IDF)consensus worldwide definition of the metabolic syndrome,522 patients and healthy subjects(273 men and 249 women,mean age 51.5±12.9 years)were enrolled and divided into 4 groups based on the amount of the component of MS,including control group,subgroup 1 with 1 component,subgroup 2 with 2 components and subgroup 3 with 3 or above components.Carotid-femoral pulse wave velocity(CFPWV)as an index reflecting large artery stiffness was measured by automatic PWV measuring system,and multiple regression analysis was performed in CFPWV and other correlative parameters. Results Compared with subjects in control group,subjects in MS subgroup 1,subgroup 2 and subgroup 3 had higher level of CFPWV(p<0.01 and 0.001 respectively),and the differences of CFPWV between subgroup 3 and subgroup 1,2 were significant(p<0.05).CFPWV was significantly correlated with age(r=0.432,p<0.001),systolic blood pressure(r=0.341,p<0.001),fasting plasma glucose(r=0.257,p<0.001), triglyceride(r=0.103,P=0.019) and waist(r=0.151,P=0.001),and stepwise multiple regression analysis demonstrated that age,systolic blood pressure and fasting plasma glucose were positively and independently related with CFPWV. Conclusions The clustering of components of MS may accelerate the occurrence and development of arterial stiffness.Measuring CFPWV as early as possible is helpful to primary prevention of cardiovascular events in the patients with components of metabolic syndrome.

Abstract:Aim To elucidate the relationship between lipoprotein lipase(LPL) gene HindⅢ polymorphism and plasma lipid profiles and HDL subclasses in obesity. Methods LPL gene HindⅢ polymorphism was assayed by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP).The subclasses of serum HDL in 95 obese subjects and 144 nonobese subjects were determined by two-dimensional gel electrophoresis conjunction with immunodetection method. Results Both in obese group and control group,the H~+H~+ homozygote and H~+ allele were the major allelotype.There was no statistically significant difference in frequencies of genotypes or alleles between two groups.Obese group had higher plasma triglycerides,apoB₁₀₀,apoCⅡ,apoCⅢ,apoE,preβ1-HDL levels and TG/HDLC,but lower HDLC,apoAI,HDL2b,apoE/CⅢ compared with control group(p<0.05).In obese group,HindⅢ H~+H~+ had higher plasma triglycerides than H~-H~-genotype.Compared with H~-H~-genotype,the subjects with H~+H~+ and H~+H~-genotypes had higher apoB₁₀₀,preβ1-HDL,HDL3b levels but lower apoE/CⅢI,HDL2a,HDL2b.In control group,the genotypes of H~+H~+ and H~+H~-showed higher apoCⅡ,apoCⅢ,HDL3b levels,but lower apoE/CⅢ,HDL2a,HDL2b levels compared with the genotype of H~-H~-(p<0.05). Conclusions H~+H~+ genotype was associated with higher plasma TG levels of obesity.LPL gene polymorphism was associated with plasma levels as well as associated with changes of HDL subclasses distribution in Chinese population.And the particle size of HDL tended to be smaller in H~+ allele carrier' subjects,furthermore,the tendency was more obvious in obese group,which indicated that HDL maturation might be abnormal in subjects with H~+ allele.