Abstract:Aim To observe the change of endothelin content and to explore the effects of vascular calcification on endothelin expression on the model of vascular calcification in rats induced by vitamin D 3 plus nicotine and calcified vascular smooth muscle cells induced by β glycerophosphate. Methods Arterial calcification of Sprague Dawley rats was induced by vitamin D 3 plus nicotine (VDN). Calcification of cultured rat vascular smooth muscle cells (VSMCs) was prepared by incubation with β glycerophosphate. Calcification was confirmed by Von Kossa staining, measurerment of calcium content, 45 Ca 2+ accumulation and alkaline phosphatase (ALP) activity of intracellular and vascular tissue. Endothelin levels in the plasma, vascular tissue and medium were measured by using radioimmunoassary. Endothelin mRNA level was determined by using competitive quantitative reverse transcription polymerase chain reaction. Results The results showed that the content of calcium, 45 Ca 2+ uptake and alkaline phosphatases activity in calcified VSMCs were increased by 118%, 174% and 7 fold respectively (all p<0.01), compared with control VSMCs. Content of endothelin in medium was increased by 35% (p<0.01). It was found that the amount of endothelin mRNA was elevated by 120% (p<0.01) compared with control. The calcium content, 45 Ca 2+ accumulation and ALP activity in calcified arteries were increased by 5.0 fold, 1.4 fold and 1.4 fold respectively (p<0.01), compared with control. Furthermore, it was showed that endothelin 1 levels in plasma and arteries tissues increased 102% and 103% respectively, compared with control (p<0.01). The amount of endothelin mRNA in calcified aorta was elevated by 22% (p<0.01) compared with control. However, the content of calcium, 45 Ca 2+ uptake and ALP activity in VDN plus endothelin receptor inhibitor groups were decreased by 33%, 36.7% and 40.4% respectively (p<0.01), compared with VDN group alone. Conclusions These results showed that in calcified artery and VSMCs the production of endothelin was increased,and the gene expression of endothelin was up regulated. The Bosentan (inhibitor of endothelin receptor) significantly reduced the vascular calcification. These results suggested that endothelin could play a role in the pathogenesis of vascular calcification.

Abstract:Aim To explore the mechanisms that heat shock proteins protected cardiomyocytes against apoptosis induced by hydrogen peroxide (H 2O 2). Methods The expression of heat shock protein 70 and αB crystallin in neonatal rat cardiomyocytes were induced by heat shock response (42℃, 1 h, and recovery for different durations). Cardiomyocyte apoptosis induced by 0.5 mmol/L hydrogen peroxide (H 2O 2) was determined by flow cytometric analysis. The activities of caspase 3, caspase 8, caspase 9 were assayed by caspase colorimetric assay kit and Western blot. The release of cytochrome C from mitochondria was observed by isolation of cellular components and Western blot. Results The expression of HSP70 and αB crystallin in neonatal rat cardiomyocytes significantly increased at 3 h and reached peak at 6～12 h after heat shock response. Heat shock response could inhibite H 2O 2 induced release of cytochrome c from mitochondria to cytoplasm, activation of caspase 3, caspase 8, caspase 9, and subsequent apoptosis in cultured neonatal rat cardiomyocytes. Conclusions HSPs protected cardiomyocytes from apoptosis by inhibiting the activation of both mitochondrial and death receptor pathways.

Abstract:Aim To investigate expression of ubiquitin conjugating enzyme (Ubc E₂) and p53 in the apoptosis of human monocyte cell line U937 induced by oxidized low density lipoprotein (ox LDL). Methods U937 cells were incubated with ox LDL. The apoptotic cells were determined by DNA fragment analysis and flow cytometric analysis. The level of p53 and ubiquitin conjugating enzyme mRNA were quantified by reverse transcription polymerase chain reaction (RT PCR). The protein contents of ubiquitin conjugating enzyme, P53 and apolipoprotein B (apo B) were analyzed by immunofluoresence staining and flow cytometric method. Results The results showed that the increase of the degree of U937 cell apoptosis was concentration dependent. Ox LDL could down regulate the gene/protein expression of ubiquitin conjugating enzyme and up regulate the gene/protein expression of P53, meanwhile, the apo B accumulated in U937 cells. Conclusion The results implicated that ox LDL induced U937 cell apoptosis by accumulation of P53 and apo B through down regulating ubiquitin conjugating enzyme. Cellular defense system, either dependent or independent on the ubiquitin system, was weakened by the ox LDL induced toxicity.

Abstract:Aim To study the effects of naked DNA encoding basic fibroblast growth factor (bFGF) for treatment acute myocardial infarction in rabbits model. Methods 42 rabbits underwent left thoracotomy followed by the ligation of left anterior descending coronary artery. After model reproducing, the rabbits were randomized to receive a directly intramyocardial injection of either pcDNA3 bFGF (n=19) or pcDNA3 (n=18). 2, 6 or 12 weeks later, immunhistologic analysis was performed to study expression of bFGF gene at protein level. Histologic analysis was performed to evaluate angiogenesis induced by gene therapy. Observing the changes of artery wall by pathology image analysis. Results Changes of electrocardiogram testify that the model of AMI is successful. immunuhistologic analysis shows that bFGF gene can express in ischemic myocardial in 6 weeks. Histologic analysis shows:there was a significant increase in the density of capillaries and anterioles in gene therapy group. Calculated the average wall thickness of the big vessels (diameter≥200 μm ) and the ratios of average wall thickness and vessel diameter by image analysis. In bFGF and control groups the average wall thickness 6W were:19.8±9.9 μm vs 18.9±9.6 μm, p>0.05; 12W: 28.3±11.5 μm vs 24.1±11.3 μm, p<0.01, respectively; ratios of 6W: 0.31±0.16, 0.24±0.12, p<0.01; 12W: 0.34±0.15,0.25±0.09,p<0.01. Conclusion Directly intramyocardial injection of bFGF gene can promote angiogenesis and induce vascular remodeling in ischemic myocardium. Suggesting that bFGF gene may have the possibility to become a new treatment strategy for coronary heart disease.

Abstract:Aim To detect the effect of neuropeptide Y (NPY) on the expression of low density lipoprotein receptors (LDLR) in human vascular smooth muscle cells (hVSMC). Methods The cultured hVSMC in vitro were divided into the control groups and the different concentration NPY groups (the concentrations of NPY were 10 8 mol/L, 10 7 mol/L, 10 6 mol/L and 10 5 mol/L). All groups were cultured for 6 h, 12 h, 24 h and 48 h respectively, then, were stained by the immunofluorescent histochemical staining and quantitatively assayed the effect of NPY on the expression of LDLR in hVSMC under laser scanning confocal microscope. Results The averaged fluorescent values of the LDLR expression in hVSMC of control groups were 2 428 to 2 527, and there were no significant differences among the different culture times (p>0.05), while there were significant differences between the averaged fluorescent values in NPY groups and those in control groups (p<0.05 or p<0.01). The averaged fluorescent values were 1 798 to 2 408 in 10 8 mol/L NPY groups, 1 783 to 2 332 in 10 7 mol/L NPY groups, 1 722 to 2 281 in 10 6 mol/L NPY groups and 1 590 to 2 010 in 10 5 mol/L NPY groups during the different culture times, decreasing averagely by 15.59%, 19.78%, 21.91% and 26.83% compared with control groups respectively, and there were significant differences among most of the different concentration NPY groups (p<0.01). NPY donwregulated the expression of LDLR in hVSMC with dose dependent and time dependent manner. Conclusion Neuropeptide Y could downregulate the expression of LDLR in hVSMC, then it probably resulted in blocking the LDLR mediated pathway, consequently LDL could accumulated in the vascular wall. This might be the important mechanism that neurofluid factor participated in the occurrence of atherosclerosis.

Abstract:Aim To investigate the effects of losartan, captopril and combined administration on the atherosclerotic renal vascular disease, so as to discover the anti atherosclerotic mechanism of these two drugs. Methods Serum nitric oxide (NO), tissue plasminogen activator(t PA), inhibitor of t PA and angiotensin converting enzyme were detected by chemical method; endothelin (ET) and angiotnesin Ⅱ were detected by radioimmuno assay. The apoptosis of vascular smooth muscle cells (VSMC) was determined by cytometry technique; Expression of CD68 protein were detected by immunohistochemical method; the expression levels of MMP1 and TIMP1 mRNA were examined by reverse transcription polymerase chain reaction. Results Losartan and captopril had no influence on serum lipid, creatine and BUN. Losartan alone and combined use with captopril could lower blood pressure significantly. The degree of renal and aortic atherosclerosis had good correlation. Compared with cholesterol diet group, losartan and combined drug administration group had smaller renal intimal area ratio (p<0.05), lower cholesterol contents in the renal atherosclerotic plaque (p<0.05), higher apoptosis percentage of VSMC (p<0.01) and lower levels of the expressions of CD68 protein (p<0.05) and MMP1 mRNA. Losartan may also elevate serum content of t PA(p<0.05). Conclusions Losartan and captopril can influence the pathogenesis of renal atherosclerosis by lowering blood pressure, enhancing apoptosis of VSMC, improving endothelial function, increasing fibrolysic function and stabilizing atherosclerotic plaque.

Abstract:Aim To study the action of ATP binding cassette transporter A1 (ABCA1) on cholesterol efflux in THP 1 macrophage derived foam cell. Methods After exposure of the cultured THP 1 macrophage derived foam cell to 22(R) hydroxycholesterol and 4,4' diisothiocyanostilbene 2,2' disulfonic acid (DIDS) at different time, cholesterol efflux and ABCA1 protein level were determined by FJ 2107P type liquid scintillator and flow cytometer, respectively. Results 22(R) hydroxycholesterol increased cholesterol efflux in THP 1 macrophage derived foam cell with time dependent pattern and DIDS inhibited cholesterol efflux in THP 1 macrophage derived foam cell with time dependent pattern; flow cytometer showed that exposure of the cultured THP 1 macrophage derived foam cell to 22(R) hydroxycholesterol and DIDS at different time, resulted in increase and decrease in the expression of ABCA1 protein in THP 1 macrophage derived foam cell with time dependent pattern, respectively. Conclusion ABCA1 play an important role in cholesterol efflux in THP 1 macrophage derived foam cell.

Abstract:Aim To clarify the content of antioxidant vitamins and oxidative property in small dense low density lipoprotein (sLDL) and to explore the role of small dense low density lipoprotein in lipid peroxidation of vascular endothelial cell. Methods Small dense low density lipoprotein was obtained by two sequential gradient ultra centrifugation and observed by negative staining electron microscopy; the content antioxidant vitamins such as vitamin A,alpha tocopherol (vitamin E) and beta carotene were measured by high performance liquid chromatography (HPLC). Continuously monitor small dense Low density lipoprotein susceptibility curve at absorbance 234 nm mediated by Cu 2+ . After exposure to small dense low density lipoprotein in vascular endothelial cell the malondialdehyde was measured. Results The small dense low density lipoprotein was isolated successfully. Compared with large buoyant low density lipoprotein, vitamin A,alpha tocopherol (vitamin E) and beta carotene and total antioxidant capacity of sLDL was 65%, 39% and 24% respectively lower and its lag phase was 37.5% lower, but its thiobarbituric acid reacting substances (TBARS) was 1.7 higher, while the the propgagtion phase was 1.28 longer. The malondialdehyde (MDA) content in culture media of 50 mg, 100 mg and 150 mg sLDL groups in 24 hour were significantly higher than those of the same dosage of large buoyant Low density lipoprotein (p<0.05). Conclusion The results suggest sLDL has strong effects on pathogenesis of atherosclerosis which may be related to decreased antioxidant content and antioxidation property and increased susceptibility to oxidation, as well as promoting peroxidation injure of vascular endothelial cell.

Abstract:Aim To examine the effect of the antisense or/and decoy oligonucleotide of nuclear factor κB (NF κB) on balloon injured intercellular adhesive molecular 1 (ICAM 1) and monocytes chemotactic protein 1 (MCP 1) in the carotid artery of rats in vivo. Methods Sprague Dawley rats underwent balloon dilation injury of the left carotid artery. Rats was divided into 7 groups (n=18) and each group included 6 time points (6 hours and 1,3,5,7,14 days) (n=3). Uninjured artery of the same rat was used to be control. Results In model group, sense group and scramble group, vessel intima area, media area and intima/media ratio increased after 5 days and reached the maximum after 14 days. Whereas lumen area decreased with different time points. Antisense group, decoy group, antisense plus decoy group improved these observational index (p<0.05). The effect of antisense plus decoy group was more obvious than that of antisense group and decoy group alone. ICAM 1 and MCP 1 mRNA expression were examined after 6 hours of artery injury, but not evident after 1 days. They increased expression continuously after 3,5 and 7 days and decreased after 14 days. Comparing with model group, sense group and scramble group, antisense group, decoy group and antisense plus decoy group all lowered ICAM 1 and MCP 1 mRNA expression in every time point (p<0.05). Immunohistochemistry studies revealed ICAM 1 and MCP 1 protein were positive stain within six time points and maximal after 14 days. In antisense group, decoy group and antisense plus decoy group, ICAM 1 and MCP 1 protein synthesis decreased in every time point comparing with model group, sense group and scramble group. Western blot studies showed NF κB p65 was disperse positive stain after 6 hours of injury and increased after 1 day and reached the peak, but protein expression was weak after 14 days. Antisense group, decoy group and antisense plus decoy group treatment inhibited protein synthesis more significantly than those of model group, sense group and scramble group(p<0.05). Conclusions NF κB modulated genes expression and protein synthesis of ICAM 1 and MCP 1; Celluar proliferation in vessel wall was dynamic change after balloon angioplasty injury; Antisense and decoy oligonucleotide of NF κB by local lipofectamine transfer inhibited NF κB activating genes modulation and the combined effect were remarkable than alone.

Abstract:Aim To investigate the effect of homocysteine on interleukin 8 production in endothelial cells, and the effect of folic acid and taurine on the role of homocysteine. Methods Human umbilical vein endothelial cells were incubated with homocysteine at a same concentration for different time or at increasing concentrations but for a same duration, and were incubated with homocysteine and folic acid or taurine for different time, then the interleukin 8 protein in the culture medium were determined by enzyme linked immunosorbent assay (ELISA). Results Enzyme linked immunosorbent assay showed that exposure of cells to homocysteine (0.1 mmol/L) for 4, 6, 8 and 12 hours, resulted in a 1.85 fold, a 1.88 fold, a 2.22 fold and a 1.56 fold increase respectively in interleukin 8 production, compared with the control group (p<0.01); meanwhile, exposure of cells to homocysteine at different concentrations (0.05 mmol/L, 0.1 mmol/L, 0.5 mmol/L and 1 mmol/L) for 8 hours, resulted in a 1.43 fold, a 2.16 fold, a 2.57 fold and a 2.88 fold increase respectively in secretion of interleukin 8, compared with the control group (p<0.05 or p<0.01 ); however, exposure of cells to homocysteine (0.1 mmol/L) and folic acid (0.05 mmol/L) or taurine (5 mmol/L) for different time, resulted in no signifcant difference in interleukin 8 production between groups. Conclusion Homocysteine induces secretion of interleukin 8 in cultured endothelial cells; and this role can be inhibited by folic acid and taurine.

Abstract:Aim To study the effects of neferine (Nef) on constraction of the rabbit basilaris arteria Induced by phenylephrine (Phe). Methods The blood vessel tension responses to drug were measured by rabbit basilaris arteria rings (RBAR) endothelium being removed and intact endothelium in vitro. Results The RBAR precontracted with Phe can be relaxed by Nef with a significant difference from saline control group (p<0.001). The vasodilatation of Nef was not significantly differences between the endothelium removed and intact endothelium groups (p>0.05). Conclusions The RBAR precontracted with Phe can be relaxed by Nef in vitro. The vasodilatation of Nef is independent of endothelium.

Abstract:Aim This study examines the relationship between PPAR gamma and delta and cholesterol efflux mediated by high density lipoprotein. Methods Pooled plasma were collected from health human. Component (density 1.063 1.21 g/cm 3) was prepared by density ultracentrifugation. U937 cells were treated by cholesterol for 24 h, cell pellets were washed with PBS, then added RPMI 1640 supplemented with 1% FBS. The cells were treated by the antisense PPAR gamma and delta oligo DNA, PPAR gamma activator ciglitazone, and PPAR responsive element decoy, respectively. The effects of the oligo DNA on efflux of cholesterol was evaluated by relative radioactivity of the cell pellets. PPAR gamma and delta protein expression levels were assayed by Western blot. Results The results demonstrated that HDL promoted cellular cholesterol efflux in dose and time dependent manner reflected by radioactivity of cell pellets. It was also observed an increase in HDL mediated cholesterol efflux associated with a decrease of antisense oligo DNA of PPAR gamma, and an decrease in HDL mediated cholesterol efflux associated with decrease of antisense oligo DNA of PPAR delta, both in a dose dependent manner. PPAR activator ciglitazone stimulated the HDL mediated cholesterol efflux. Treatment with PPAR responsive element decoy inhibited the cholesterol efflux mediated by HDL. Western blot assay demonstrated that PPARgamma protein level was increased, while PPARdelta level decreased by HDL. Conclusion This study suggests that PPAR gamma may improve the cholesterol efflux mediated by HDL, PPAR delta may prevent the HDL mediated cholesterol efflux.

Abstract:Aim To study whether lipopolysaccharide(LPS) regulates the production of matrix metalloproteinase 1(MMP 1) and tissue inhibitor of matrix metalloproteinase 1 (TIMP 1) in fetal aortic smooth muscle cells. Methods Aortic smooth muscle cells from 4～6month healthy abortive fetuses were incubated for 72 h with various concentration of LPS in vitro (0, 5, 10, 25 mg/L). The concentration of MMP 1 and TIMP 1 in the concentrated culture media was measured by Western Blotting. Results Compared with the control group, LPS could inhibit the production of MMP 1 in the smooth muscle cells, but could not change the production of TIMP 1 in the smooth muscle cells. Conclusions LPS could not promote the rupture of the atherosclerotic plaques by destroying the balance of the MMP 1 and TIMP 1 in the smooth muscle cells.

Abstract:Aim To observe the inhibitory effect of different doses 32 P radiation on the neointimal hyperplasia and stenosis of antologous vein graft. Methods Thirty rabbits underwent 32 P radiotherapy with different doses of 2,4,8,16 μCi/cm 2. HE staining, proliferating cell nuclear antigen immunohistochemical method and computer imaging analysis technique were performed. The neointimal area, the smooth muscle cell (SMC) proliferation index and vessel cavities lost rate were analyzed. Results No neointima was observed in 16 μCi/cm 2 group, but necrosis of most vessel wall cells occurred and the vessels were injured seriously. Thin neointima was formed in 8 μCi/cm 2 group. The neointimal area, SMC proliferation index and cavities lost rate were less than in the control group. There was no significant difference in the parameters between the 2 μCi/cm 2 group, 4 μCi/cm 2 group and control group. Conclusion Low dose 32 P radiation could effectively inhibit the neointimal hyperplasia and restenosis of autologous vein grafts, and the suitable dose was 8 μCi/cm 2 in this model.

Abstract:Aim To investigate the effects of advanced glycation end product (AGE) on the proliferative activity of vascular smooth muscle cell (VSMC) of rats. Methods In this study, Type Ⅰ Collagen AGE and Bovine serum albumin AGE was prepared in vitro. Cultured VSMC were obtained from rat abdominal aorta and used between passage 3 and 4, then stimulated with AGE. The control groups were stimulated with Type Ⅰ Collagen and bovine serum albumin. At the same time, anti vascular endothelial growth factor (VEGF) antibody was added in cells. 3H TdR incorporation into cultured cells was used as a parameter for cell proliferation. Results Type Ⅰ Collagen AGE caused the increase in 3 H TdR incorporation of cells compared with Type Ⅰ Collagen, which was abrogated by anti VEGF antibody. But bovine serum albumin AGE reduced the proliferation of cells, and anti VEGF antibody didn't affect cell proliferation. Conclusion The effects of Type Ⅰ Collagen AGE and bovine serum albumin AGE to the proliferation of VSMC and secretion of VEGF on VSMC are different.

Abstract:Aim To investigate the effect of lovastatin on secretion of matrix metalloproteinase 3 (MMP 3) in cultured vascular smooth muscle cells (VSMC) of rabbits. Methods Expression of MMP 3 was detected by Western blot, AP 1 binding activity was detected by electrophoretic mobility shift assay (EMSA), mRNA level of MMP 3 was detected by reverse transcription polymerase chain reaction (RT PCR). Results Interleukin 1α (IL 1α) combined with platelet derived growth factor BB (PDGF BB) strongly increased the expression of MMP 3 at VSMC. Lovastatin inhibited the upregulated expression of MMP 3 by IL 1α and PDGF BB in a concentration dependent manner. This inhibitory effect was reversed by mevalonate and GGPP, but not by squalene. Lovastatin decreased AP 1 binding activity enhanced by IL 1α and PDGF BB, but had no significant effect on MMP 3 mRNA level. Conclusion Lovastatin inhibited MMP 3 secretion at VSMC, which could contribute to its plaque stablising effects.

Abstract:Aim To study the effect of low density lipoprotein (LDL), oxidized low density lipoprotein (ox LDL), high density lipoprotein (HDL), oxidized high density lipoprotein (ox HDL)on the expression of ATP binding cassette transporter 1 (ABC1) mRNA in THP 1 cells. Methods Cultured THP 1 cells were induced into macrophage by 40 μg/L phorbol ester (PMA)for 48 h and then incubated with 20 mg/L and 120 mg/L LDL, ox LDL, HDL and ox HDL for 24 h, total RNA of THP 1 cells were abstracted, reverse transcription polymerase chain reaction (RT PCR) were performed to inspect of the expression of ABC1 mRNA. Results The expression of ABC1 mRNA in THP 1 cells increased mildly in the presence of low dose of LDL, ox LDL and ox HDL, and low dose of HDL showed almost no effect on ABC1 expression; on the contrary, the expression of ABC1 mRNA decreased obviously in the presence of high dose of LDL, ox LDL and ox HDL, while HDL caused a mildly decrease in ABC1 mRNA expression in THP 1 cells. Conclusions Low dose of LDL, ox LDL and ox HDL can increase the expression of ABC1 mRNA in THP 1 cells; while high dose of LDL, ox LDL, HDL and ox HDL suppress ABC1 mRNA expression in THP 1 cells. This may imply that the effect of different levels of lipoproteins and oxidized lipoproteins on ABC1 expression play an important role in atherogenesis.

Abstract:Aim To investigate the relationships between -75 bp / +83 bp polymorphism in apolipoprotein(apo)A1 gene, lipids levels and the occurrence of coronary atherosclerosis disease(CAD). Methods The distributions of two MspI polymorphisms of the apo A1 gene, -75 bp and +83 bp, and blood lipids levels were determined among 137 Chinese patients in relation to circulating lipids and coronary angiography. Results The control group had higher M 1-/M 2- frequencies than the coronary atherosclerosis disease group (M 1: p<0.005; M 2: p<0.05) and the M 1- and M 2- alleles were associated with increased high density lipoprotein (M 1-: p<0.0001; M 2-: p<0.05) and apo A1 (M 1-: p<0.0001; M 2-: p<0.05) levels. M 1- and M 2- were significantly correlated with CAD (p<0.01 and p<0.05, respectively). Conclusions The results suggest that the base changes from G to A at the -75 bp site and C to T/G to A at the +83 bp site do have increased circulating levels of apo A1 and high density lipoprotein and that individuals with these base changes are likely to have a reduced risk of developing CAD.

Abstract:Aim To investigate the roles of inflammatory mediators in the pathogenesis of acute myocardial infarction (AMI). Methods Inflammatory mediators such as C reactive protein (CRP), tumor necrosis factor α (TNF α), and fibrinogen on the 1st, 4th, 7 th day and 2 months later of onset were measured in twenty nine cases with AMI. Results Concentrations of CRP did not show difference compared with the controls on the 1st day, but increased remarkably on the 4th day, and decreased on the 7th day. It normalized 2 months later. TNF α could only be detected in 6 samples among which 3 in control group and 3 in AMI group. Concentrations of fibrinogen increased on the 1st day, and continued increasing on the 4th and 7th day. It normalized 2 months later. Conclusions Changes of CRP was not the initiator of AMI but the reaction following AMI. The very low detectable rate of TNF α made it of little value as a risk factor of AMI. Fibrinogen might play roles in the pathogenesis of AMI.

Abstract:Aim To study the association between angiotensin converting enzyme (ACE) gene polymorphism and ACE activity,angiotensin Ⅱ (AngⅡ) in coronary artery disease patients. Methods The serum ACE activity and plasma AngⅡ level in 76 patients with coronary artery disease and 68 healthy subjects were measured. The relation between serum ACE activity and plasma AngⅡ level was analyzed by linear regression. Results The serum ACE activity and plasma AngⅡ level were similar in coronary artery disease and control groups. But the serum ACE activity in different genotypes was significantly different in the two groups. The serum ACE activity in DD genotype (homozygotes for the deletion) was markedly higher than in ID genotypes (heterozygotes) and II genotypes (homozygotes for the insertion). The plasma AngⅡ level was similar in different genotypes in the two groups. No correlation was found between serum ACE activity and plasma AngⅡ level. Conclusion The ACE gene insertion/deletion polymorphism is the important factor that influenced the serum ACE activity. However it has no influence on plasma AngⅡ level. There is no relationship between the serum ACE activity and plasma AngⅡ level. The findings suggest the mechanism that ACE insertion/deletion polymorphism contribute to the generation or development of coronary artery disease is not completed by increasing plasma AngⅡ level.

Abstract:Aim To study the influential factors that lead to form coronary collateral circulation. Methods The date of coronary angiography and clinical characteristics were analysed in 253 cases with coronary heart disease(CHD) underwent coronary angiography [coronary collateral circulation was present in 122 patients (Forming collateral circulation group) and absent in 131 patients as control group(No collateral circulation group). [WTHZ]Results 98.36% of patients in the forming collateral circulation group presented complete or sub total occlusion of coronary artery . The multiple vessel occlusion rate and complete occlusion rate of coronary artery were significantly higher in the forming collateral circulation group than those of the no collaterai circulation group(30.00% vs 11.45%,p<0.001;75.77% vs 60.27%, p<0.05,individually). The rate of forming collateral was higher in the vessels with complete occlusion than those of sud total occlusion(58.09% vs 40.20%,p<0.05). Multivariate logistic regression analysis showed that vassel occlusion number and degree were two significant variables associated with collateral circulation.The level of serum total cholesterol and abnormal rate of serum triglycerin were significantly higher in the no collateral circulation group than those of the forming collateral circulation group (5.03±1.38 mmol/L vs 4.68± 1.06 mmol/L,p<0.05; 45.80% vs 32.78%,p<0.05). Conclusion The serious degree of coronary occlusion lesion is great important factors of whether forming coronary collateral circulation. Hyperlipidemia is not good for the formation of coronary collateral circulation.

Abstract:Aim To evaluate the safety and therapeutic effects of direct percutaneous transluminal coronary angioplasty (PTCA) in treatment of acute myocardial infarction (AMI), and compare the effects vs thrombolytic therapy. Methods 62 AMI patients without thrombolytic therapy were treated by direct PTCA after urgent coronary angiography, 59 AMI patients were treated by thrombolytic therapy. The safety and therapeutic effects of direct PTCA were studied and compared with thrombolytic therapy. Results In direct PTCA group, 60 cases were reperfused (96.7%), among which 4 were complicated with cardiogenic shock and the blood pressure raised to normal, 1 case was complicated with acute upper gastrointestinal hemorrhage, no mortality; whereas, in thrombolytic treatment group, 38 cases were reperfused (64.4%), 5 died in hospital and 2 died after discharge; 1 patient complicated with acute upper gastrointestinal hemorrhage, 1 with hematuria and 5 with cardiogenic shock; the motality was 11.9%. The rate of reperfusion in direct PTCA group was higher than that of thrombolytic therapy group; meanwhile, the incidence of major cardiac events in direct PTCA group was significantly lower than that of thrombolytic therapy (p<0.01). Conclusions Direct PTCA for treatment of AMI was safe and effective; the rate of reperfusion after direct PTCA was higher than that of thrombolytic therapy; thus, the therapeutic effects and the prognosis of direct PTCA was better than those of thrombolytic therapy.

Abstract:Aim To investigate the effect and the heart protecting mechanism of manshuailing oral liquid on plasma soluble intercellular adhesion molecular 1 (sICAM 1) level in patients with congestive heart failure (CHF). Methods 120 patients of CHF were randomly divided into 2 groups. 60 cases in the routine treatment group received common therapy, and 60 cases in the manshunailing oral liquid treatment group were treated with additional manshuailing oral liquid except common therapy. 40 normal cases were taken as the control group. The plasma level of sICAM 1 was tested before and after 4 weeks management by enzyme linked immunosorbent assay (ELISA) method. Results The plasma concentration of sICAM 1 in both the treatment groups was higher than the control group even after treating (p<0.01). Compared with that of pretreating, the level of sICAM 1 decreased in both the treatment groups (p<0.01), but the magnitude of change was greater in the manshuailing oral liquid group than in the routine treatment group (p<0.01). Conclusion Manshuailing oral liquid may inhibit ventricular remodeling and improve heart function by decreasing the concentration of sICAM 1 in patients with CHF.