Abstract:Aim To study the effects of stichopus variegates compound on the iliac arterial endothelial function and ultrastructure of rabbits after transluminal balloon angioplasty (TBA) of iliac atherosclerosis model. Methods 50 purebred New Zealand rabbits were randomly divided into four groups: Stichopus,Simvastatin,model and normal group. Endothelium of iliac arteries in the front three groups were denuded by balloon catheter and fed with 2% cholesterol,3% lard and 3% yolk mixed forage for six weeks,and then,atherosclerotic stenosis was showed by iliac angiography. Stichopus group [0.5 g/(kg·d)] and Simvastatin group [0.5 mg/(kg·d)] were fed by gastric canal in mouth cavity. At the same time NaCl solution (0.9%) were fed in model group. All the rabbits were fed in different cages and not limited drinking. After four weeks since TBA,blood was collected from left carotid artery to measure the changes of concentrations of endothelin (ET) and nitric oxide(NO). Results ①After four weeks since TBA,the concentrations of plasm ET in model groups were higher than the one in the Simvastatin and Stichopus groups,and the concentrations of serum NO decreased obviously; the concentrations of plasm ET in Stichopus groups had an increasing tendency compared with Simvastatin and normal groups. ②After four weeks since TBA,neointimal mean thickness of segment operated TBA in model groups increased significantly,compared with Simvastatin and Stichopus groups. There were greater extent of lumen stenosis in model groups than the one in Simvastatin and Stichopus groups. ③Compared with model groups there were small vessel smooth muscle cell body and nucleus,less organelles and more myofilament contents,better cell differentiation,and less lipid droplet were phagocyted in Simvastatin and Stichopus groups under the transmission electron microscope. ④There were less platelets adherence in Simvastatin and Stichopus groups under scanning electron microscope. Conclusion Stichopus variegatus compound can significantly inhibit vessel smooth muscle cells proliferation,lessen neointimal thickness,enlarge luminal areas,decrease extent of lumen stenosis and protect endothelial function after iliac arterial transluminal angioplasty of rabbits.

Abstract:Aim To discuss the function of very low density lipoprotein (VLDL) in foam cell formation and the role of VLDL receptor (VLDLR) in this process. Methods Macrophage cells separated from mouse abdominal cavity were incubated with three lipoproteins, VLDL, β-VLDL, and low density lipoprotein (LDL) for 24 h, 48 h respectively. The content of triglyceride (TG) and total cholesterol (TC) in cells was examined, and the foam cells formation was identified by oil red O dying. The mRNA expression level of LDLR, LRP and VLDLR was measured by half-quantitation RT-PCR. Results The content of TG and TC increased by all three lipoprotein; VLDLR was upregulated by VLDL and β-VLDL while LDLR was downregulated and LRP was upregulated a little. Conclusion The experiment in the ldl-a7-VR cells which can steadily express VLDLR shows that the uptake of triglyceride-rich lipoprotein (TRL) mediated by VLDLR plays an important role in the accumulation of lipids and the foam cell formation.

Abstract:Aim To study the expression of hypoxia-inducible factor-1α (HIF-1α) and related genes in abdominal aorta aneurysm (AAA). Methods 22 AAA specimens were collected and 6 normal abdominal aorta tissue were used as control. Northern blot was used to evaluate the expression of HIF-1α mRNA. Western blot and immunohistochemistry method was used to determine the expression of HIF-1α, vascular endothelial growth factor (VEGF) and erythropoietin (EPO). Microvessel density(MVD) was also studied. Results The expression of HIF-1α was significantly higher in AAA than that in normal abdominal aorta (p<0.01). The expression of VEGF and EPO were also higher in AAA (p<0.01). Most of the positive cells located in VSMC and adventitia of AAA. The MVD counts were higher in AAA. Conclusion HIF-1α may have an important role in the onset of AAA, which may be obtained by promoting the expression of VEGF and EPO.

Abstract:Aim To explore the effects of Li Shui Tiao Zhi Capsule (LSTZ) on monocyte chemoattractant protein-1 (MCP-1) of vascular smooth muscle cells (VSMC) and P-selectin of vascular endothelial cells (EC) induced by minilly modified low density lipoprotein (mm-LDL). Methods Cells were treated by different concentrations of serum-containing LSTZ (5%,10% and 20%) and mm-LDL. MCP-1 of VSMC was determined with ELISA. P-selectin of EC was detected with Cell-ELISA. Results The expression of MCP-1 induced by mm-LDL (20 mg/L) can be reduced by 20% serum-containing LSTZ (p<0.05). The expression of P-selectin induced by mm-LDL (40 mg/L) was suppressed by 10% serum-containing LSTZ (p<0.05), and it showed a notably inhibition on concentration of 20% (p<0.01). Conclusions Protecting vascular cell and relieving respone of inflammation may be one of the mechanisms of anti-atherosclerosis of LSTZ. Not only MCP-1 but also P-selectin may be involved in the “XUEYUZHENG" in Chinese Medical theory.

Abstract:Aim To observe the effect of Recipe of Removing Both Phlegm and Blood stasis on aorta and cardiac muscle of rabbits as well as ultrastructure of endothelial cells. Methods The rabbits were fed with high fat diet in order to reproduce hyperlipemia models; The endothelial cells were cultured in high fat serum to observe the effect of hyperlipemia on it. They were treated by two kinds of recipes. In this experiment the ultrastructure of endothelial cells (EC), aorta and cardiac muscle was observed through electron microscope. Results Recipe of Removing Both Phlegm and Blood stasis group: Smooth tunica intima of aorta, little formation sclerosis plaque of aorta, dense and regular arrangement of endothelial cells, recovered cell appearance, regular arrangement of cardiac muscle, slight adipose tissue infiltration in cardiac muscle, no myofilament solution and decrease of expansion of sarcoplasmic reticulum. The results showed that recipe prevented EC, aorta and cardiac muscle from injury. Conclusion Recipe of Removing Both Phlegm and Blood stasis can be used against myocardial ischemia, prevent vasospasm, platelet aggregation and arteriosclerosis.

Abstract:Aim To study the influence of thrombin receptor on the proliferation of rat vascular smooth muscle cells,probe into mechanism of antisense sequence of thrombin receptor restrained the proliferation of rat vascular smooth cells. Methods Take the incoporation of 3H-thymidine as the target to evaluate vascular smooth muscle cells proliferation; Antisense sequence of thrombin receptor restrained the expression of mRNA of thrombin receptorin vascular smooth cells was detected by RT-PCR; Antisense sequence of thrombin receptor restrained the expression of protein of thrombin receptor was detected by Western-blot; The influence of antisense sequence of thrombin receptor on phosphate inositol of vascular smooth cells was detected by incoporation of 3H-inositol. Results Antisense sequence of thrombin receptor restrained vascular smooth muscle cells proliferation marketedly (compared with control p<0.05),restrained expression of mRNA and protein of thrombin receptor marketedly;Also restrained metabolism of phosphate inositol in vascular smooth cells. Conclusion Antisense sequence of thrombin receptor restrained SD rat vascular smooth muscle cells proliferation marketedly; Antisense sequence of thrombin receptor restrained vascular smooth muscle cells proliferation which could arrested gene expression of thrombin receptor,restrained signal trasduction of vascular smooth muscle cells.

Abstract:Aim To explore the effects of high density lipoprotein 2 (HDL 2) and 3 (HDL 3) on expression of peroxisome proliferator-activated receptor γ (PPARγ)and CD36, and cellular lipid accumulation in THP-1 macrophages. Methods After exposure of the cultured THP-1 macrophages to oxidized low density lipoprotein (ox-LDL) only, and ox-LDL and HDL 2 or HDL 3, lipid accumulation was valued by high performance liquid chromatography combined with enzyme assay. The mRNA and protein expression levels of PPARγ and CD36 were determined by reverse transcription-polymerase chain reaction (RT-PCR), Western blotting, respectively. Results HDL increased PPARγ expression level and decreased expression level of CD36 in THP-1 macrophages, and reduced lipid accumulation of THP-1 cells. HDL 3 showed more potential effects of downregulating CD36, upregulating PPARγ, and decreasing cellular lipid accumulation in THP-1 macrophages than HDL 2. Conclusion The data demonstrates that both HDL 2 and HDL 3 inhibit cellular lipid accumulation induced by ox-LDL in THP-1 macrophages. Moreover the effects of HDL 3 is higher than HDL 2. The mechanism may be that HDL could inhibit cellular lipid accumulation by modulating expression of PPARγ-responsive gene, CD36, a receptor for ox-LDL.

Abstract:Aim To explore the relationship between adipophilin and atherosclerosis. Methods The New Zealand white rabbits were fed with high cholesterol chow for 12 weeks and became the model of atherosclerosis. The level of serum total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, triglyceride, and cholesterol content of aortic wall were investigated. The areas of fatty streak of the aortae were measured after staining with Sodan Ⅳ. The aortic, and live specimens with HE and immunohistochemstry staining were observed with light microscopes. Results In the animals fed with high cholesterol chow, the level of serum total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, triglyceride, and cholesterol content of aortic wall significantly increased. The areas of fatty streak in the aortae was 40.1%±7.3% at the end of 12 weeks. The fatty streak of the aorta with immunohistochemstry staining was strongly positive, and the liver was negative with or without high cholesterol chow. Conclusions The New Zealand white rabbits could be made the model of atherosclerosis through feeding with high cholesterol chow for 12 weeks. Expression of adipophilin in atherosclerotic rabbits increased,which suggested the adipophilin was related to the development of atherosclerosis.

Abstract:Aim To evaluate the distribution of induced cyclooxygenase (COX-2)expression in human coronary arteries with different atherosclerotic lesions. Methods 45 coronary arteries specimens from 15 autopsy cases were divided into 3 groups according to pathologic features of HE staining and AHA definition respectively,which were 3 healthy coronary arteries as control,22 fibrotic plaque or type Ⅴ lesion specimens (representing stable plaque),and 20 complicated plaque or type Ⅵ lesion specimens (representing unstable plaque). RT-PCR were performed for mRNA analysis,and immunohistochemical staining were used for location of protein. Results COX-2 was found in the areas of plaques but not in healthy or nonatherosclerotic vascular walls. COX-2 expression in complicated plaques was significantly higher than in fibrous plaques (COX-2 expression 147.0±1.1 vs 56.2±4.4,p<0.01). Conclusions These findings suggests that COX-2 might play a role in pathogenesis of atherosclerosis,and modulation of inflammatory process involved in plaque stability. Inhibition of COX-2 over-expression in plaque areas might be a potential approach to atherosclerosis treatment and plaque stabilization.

Abstract:Aim To investigate the effects of Simvastatin on the expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) in cultured human umbilical vein endothelial cell (hUVEC). Methods The effects of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and Simvastatin on the protein levels of VCAM-1 and ICAM-1 in hUVEC were observed by means of immunocytochemistry and Western blot. Results TNF-α and IL-1β significantly upregulated the protein levels of VCAM-1 and ICAM-1 in hUVEC,which were inhibited by Simvastatin. Conclusion Simvastatin inhibited the upregulations of VCAM-1 and ICAM-1 stimulated by proinflammatory factors, which may increase the stability of plaques and decelerate the progression of atherosclerosis.

Abstract:Aim To investigate the effect of rat peritoneal mast cell on collagen Ⅰand Ⅲ expression in foaming smooth muscle cell(SMC). Methods SMC were treated with the supernatant of mast cell completmented with 100mg/L oxidized low density lipoprotein (ox-LDL)for 48h. The mRNA expressions of collagenⅠand Ⅲ were detected by RT-PCR. Immunocytochemistry staining was used to detect the protein expression of collagen Ⅰand Ⅲ. Results With exposure to mast cell supernatant and ox-LDL, the expression of collagen Ⅰand Ⅲ in SMC decreased. Conclusions Mast cell inhibits SMC collagen Ⅰand Ⅲ expression in vitro. Our findings support the hypothesis that mediums released from activated mast cell in atherosclerotic plaques contributes to cap remodeling.

Abstract:Aim To investigate the influence of nitric oxide (NO), nitric oxide synthase (NOS) on cardiomyocyte hypoxia/reoxygenation and effects of NO on cardiomyocytes delayed protection (DP). Methods The content of NO, NOS were measured in the models of hypoxia/reoxygenation (H/R) of cultured neonatal rat cardiomyocytes. The cell viability, lactate dehydrogenase (LDH) release, and the content of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured in the models of DP of cultured neonatal rat cardiomyocytes, with pretreatment of L-NA, L-arginine, sodium nitroprusside (SNP). Results NO and NOS increased significantly after transient hypoxia/reoxygenation. Hypoxic DP attenuated cardiomyocyte injure induced by H/R. Pretreatment with non-selective NOS inhibitor L-NA abolished the protectiive effect of hypoxia DP, L-arginine can not mimicked DP, but SNP may mimicked DP. Conclusion NO may be involved in the protection mechanism of DP.

Abstract:Aim To observe the effect of grape seed proanthocyanidin extract (GSPE) on serum C-reactive protein (CRP) in rabbits. Methods 15 New Zealand male rabbits were randomized into three groups with 5 rabbits in each group. The control group was fed with standard diet. The cholesterol group was fed with standard diet containing 1% cholesterol. The GSPE group was fed with standard diet containing 1% GSPE plus 1% cholesterol. All the rabbits were fed for twelve weeks. Blood samples were drawn from ear middle arteries of rabbits just before the experiment and at the first, the second, the forth, the eighth and the twelfth weekend of the experiment. All the rabbits were fasted for at least eight hours before the blood was drawn. Serum CRP was determined using a commercially available CRP EIA kit. All the rabbits were sacrificed at the twelfth weekend and aortas of the rabbits were excised for the morphological observation. Aorta samples were observed through optical microscope. Results Compared with the cholesterol group, the serum CRP contents were lowered markedly by dietary GSPE (p<0.001) at the first weekend and lasted to the end of the experiment. Both the cholesterol group and the GSPE group showed high correlation of the treat and time (r=0.99047, p<0.001 and r=0.74777, p<0.001). The extent and severity of atherosclerosis (the thick of aortas and the number of foam cells) of the GSPE group were less than those of the cholesterol group (p<0.01). Conclusions GSPE had the efficacy of anti-atherogenesis, one mechanism of which was that it can inhibit the CRP.

Abstract:Aim To investigate the expression of connective tissue growth factor (CTGF)in the kidney of spontaneously hypertensive rats. Methods The comprised normotensive control (WKY)and hypertensive groups(SHR) were taken as the objects of study,of which blood pressure,urinary β₂-microglobulin,Bun,Scr were acquired at 12-week old and 32-week old respectively,at the same time,the renal expression of CTGF were determined,when the rat were sacrificed. Results In SHR,the blood pressure,urinary microglobulin,except Bun,Scr were significantly increased compared with age-matched controls,even in the SHR group,the urinary β₂-MP in 32-week old group were markedly increased,compared with that in 12-week old group. Semi-quantitative assessment of the immune-histochemical staining showed that renal expression of CTGF in SHR groups were significantly increased compared with that in WKY groups. Futher more,in SHR,the expression of CTGF in 32-week old group were also markedly increased compared with that in 12-week old group,and it is positively corelated with the increasing of urinary β₂-microglobulin. Conclusion Renal expression of CTGF is increased in SHR,which is possibly involved in the development of renal damage.

Abstract:Aim To investigate the effects of oxidized lipoprotein (a) [ox-Lp(a)] on the expression of macrophage inflammatory protein-1α (MIP-1α)in cultured human umbilical endothelial cells (hUVEC). Methods Native Lp(a)[n-Lp(a)] and different concentrations of ox-Lp(a) were incubated with hUVEC. Cell ELISA was used to detect the expression of MIP-1α. Monocyte adhesion assay was used to detect the Monocyte adhesion. MIP-1α mRNA expression were determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Results Ox-Lp(a) dramatically enhanced the levels of MIP-1α in a dose dependent manner, increasing MIP-1α epression in hUVEC by 121%±8% at 5 nmol/L,163%±13% at 10 nmol/L and 241%±28%at 20 nmol/L. In addition, 10 nmol/L of ox-Lp(a) for 2 h could significantly increase the amount of monocyte adherence to endothelial cells. Moreover, RT-PCR analysis demonstrated that the amount of MIP-1α mRNA increased after treatment with ox-Lp(a) for 24 h. Conclusion Ox-Lp(a) can induce MIP-1α expression in hUVEC, which may thereby influence the pathogenesis of athersclerosis.

Abstract:Aim To investigate the effects of insulin on expression and secretion of tumor necrosis factor-α (TNF-α) protein of human peripheral blood mononuclear cells and the effects of Pravastatin. Methods The human peripheral blood mononuclear cells were derived from healthy volunteer's vein blood by dendity centrifugation using Ficoll and cultured in RPMI 1640 medium containing 10% autologous serum, and then added human insulin, Pravasatatin and mevalonate to continue culture for 48 h, the levels of TNF-α protein in cells and in supernatant were tested by Western blot and ELISA assay. Results Insulin stimulation resulted in significantly elevated levels of TNF-α protein in mononuclear cells and the supernatant of cells culture in dose-dependent, however, after incubated with insulin plus Pravastain, the levels of TNF-α protein in cells and the supernatant were lower, which effects could be diminished by added mevalonate. Conclusion Insulin can increase the expression and secretion of TNF-α protein of human peripheral mononuclear cells and its effects can be inhibited by Pravastatin, which indicats that the cardioprotective effects of Pravastatin on diabetes patients might be partially associated with inhibiting inflammation mediated by insulin.

Abstract:Aim To investigate the changes of expression of basic fibroblast growth factor (bFGF) and to evaluate the effect of bFGF on angiogenesis in ischemic myocardium after acute myocardial infarction. Methods 30 male infarcted rats were divided into 24h group, 1w group, 2w group, 3w group and 4w group, expression of bFGF protein in ischemic myocardium was detected with immunohistochemical staining. Another 6 infarcted rats were treated with bFGF neutralizing antibody for 2 weeks. Capillary density and arteriolar density were detected in ischemic myocardium. Results Expression of bFGF protein in ischemic myocardium increased at 24 hours after acute myocardial infarction, and peaked at 1～2 weeks after acute myocardial infarction, while gradually decreased at 3 weeks after acute myocardial infarction. The expression of bFGF at 4 weeks after acute myocardial infarction still was above normal level. Capillary density and arteriolar density were significantly augmented at 2 weeks after acute myocardial infarction. Arteriolar density in ischemic myocardium was greatly decreased, but capillary density was in absence of change, after action of bFGF was blocked. Conclusions Expression of bFGF protein in ischemic myocardium after acute myocardial infarction was increased continuously for 1 months or more. bFGF mediates proliferation of arterioles in ischemic myocardium.

Abstract:Aim To investigate tissue factor (TF) mRNA expression in adipocytes of atherosclerotic rabbit, and the effects of fenofibrate on the expression of TF in adipocytes. Methods Male rabbits (n=15) were randomly separated into three groups. Normal group were fed with normal diet for 12 weeks, and the other two groups were fed with high-cholesterol diet for 8 weeks and then assigned to 30 mg/(kg·d) fenofibrate and placebo for 4 weeks. At the end of 12 th week from the start of experiment, subcutaneous adipose was collected for adipocytes culture under deep anesthesia. The level of TF mRNA was detected by reverse transcription-polymerase chain reaction. Results The atherogenic diet caused a consistent increase in serum levels of total cholesterol (TC) (p<0.05) and did not affect serum triglyceride (TG) levels. Fenofibrate did not change serum levels of TG and TC. In the rabbits fed with a high cholesterol diet, TF mRNA expression in adipocytes was elevated (1.081±0.011 vs. 0.939±0.018, p<0.01). Fenofibrate significantly reduced TF mRNA (0.893±0.022 vs. 1.081±0.011, p<0.01). Conclusion TF mRNA expression increases in adipocytes of atherosclerotic rabbit. Fenofibrate reduces TF expression in adipocytes,which suggests that fenofibrate may have an antithrombtic effect.

Abstract:Aim To observe the effect of granular-macrophage colony stimulating factor (GM-CSF) on the expression and activity of matrix metalloproteinases (MMP). Methods Human endothelial cells were cultured in vitro and the protein expressions of MMP-2 were detected by Western blot. MMP-2'activity was detected by Zymography. Results The results revealed that the protein expression and activity of MMP-2 were significantly increased after endothelial cells were stimulated by GM-CSF. And the protein expression and activity of MMP-2 were in a dose-dependent and time-dependent manner. Conclusions The results indicate that GM-CSF can obviously increase the protein expression and activity of MMP-2 in human endothelial cells. So GM-CSF could enhance the breakdown of matrix in lesions of atherosclerosis which could probably induce vulnerable plaque.

Abstract:Aim To investigate the relationship between total white blood cell (WBC) Count with cardiovascular risk factors in healthy subjects. Methods The age,gender and history of smoking of 138 subjects were investigated. The body mass index (BMI),waist circumference (WC), waist to hip ratio (WHR),systolic blood pressure (SBP),Diastolic blood pressure (DBP),triglyceride (TG),total cholesterol (TC),low density lipoprotein,high density lipoprotein- cholesterol (HDLC),fasting insulin,and tumour necrosis factor-α (TNF-α) were also determined. A 75 g oral glucose tolerance test was performed in all participants. Insulin resistance was evaluated by using Homeostasis Model Assessment (HOMA). Results Total WBC count was significantly positive correlation(p<0.05) with BMI,WC,WHR,SBP,DBP,TNF-α,2 h glucose after glucose load,LnTG,LnFIns,and Ln(HOMA-IRI) (all p<0.05) and negative correlation with HDLC (P=0.006). In a multiple stepwise regression analysis,only WC,TNF-α and history of smoking were positive predictors of total WBC count after adjusting for all potentially confounding variables. Conclusion The total WBC count associates with cardiovascular risk factors such as obesity,2-h glucose after load,blood pressure,TG,HDL-C and history of smoking.

Abstract:Aim To investigate the relationship between the polymorphism of apolipoprotein A5 gene 56C→G and the levels of serum lipids and lipoproteins. Methods 486 subjects were collected to determine the genotypes by using polymerase reaction-restriction fragments length polymorphisms (PCR-RFLP). Results There is only one carrier with minor allele of 56C→G, in another word, only one heterozygous was found in the group (n=468). Conclusion The relationship between the site of apolipoprotein A5 gene 56C→G and the levels of serum lipids and lipoproteins can not be established.

Abstract:Aim To analyse the mutation site in low density lipoprotein receptor (LDLR) gene of a familial hypercholesteroleia (FH) family. Methods The patients' serum lipids were analysed by enzymatic method. The peripheral whole blood was used to isolate the genomic DNA. The genomic DNAs were used as templets to amplify 18 exons of LDLR gene by polymerase chain reaction (PCR). The PCR products were analysed using polymerase chain reaction- single strand conformation polymorphism (PCR-SSCP) method and the exons showing abnormal band on PCR-SSCP were underwent DNA sequencing. Results A synonymous mutation (AGA471AGG) and a nonsense mutation (TGG483TAG) were identified by PCR-SSCP combined with DNA sequencing. The nonsense mutation (TGG483TAG) introduced a beforehand stop codon in codon 483. Conclusion A novel mutation of LDLC gene was detected by the PCR-SSCP methods.

Abstract:Aim To valuate the Association between heme oxygenase-1(HO-1)and angiographic morphology of coronary lesions in patients with coronary heart disease (CHD). Methods One hundred and thirty-six patients with coronary heart disease who underwent coronary angiography were selected in this study,and 40 patients with normal coronary artery were selected as control. According to angiographic morphology of coronary lesions,these patients were split into type I(smooth borders)group(n1=53),type Ⅱ(irregular borders)group(70)and type Ⅲ(long and irregular lesions)group(n3=13). The levels of HO-1 protein expression in monocyte and lymphocyte coming from patients with CHD were tested by immunohistochemistry and western blot. Computer picture analyzing system were also used to measure the levels of HO-1 protein expression. Results HO-1 protein is located in cell plasma; levels of HO-1 protein expression in patients with coronary heart disease were significantly higher than those of the controls(p<0.01); levels of HO-1 protein expression were the highest in type Ⅲ group,then type Ⅱ group,and at last the type I group(p<0.01). Conclusions There is a higher expression of HO-1 in patients with CHD,the levels of HO-1 protein are associated with angiographic morphology of coronary lesions,suspecting that HO-1 is associated with severity of coronary heart disease.

Abstract:Aim To evaluate the effect and explore the mechanism of the Compound Salvia Miltiorrhiza Bunge Injection on the vascular endothelium-dependent vasodilatation in patienents with CHD. Methods 84 patienents were randomly divided into three groups(n=28): all patienents were given basic therapy according to the therapeutic guide of CHD, while the two therapeutic groups were respectively added the Compound Salvia Miltiorrhiza Bunge Injection and VitC. We examined the baseline(D 0) and the flow-mediated vasodilation (FMD) of brachial artery by high-resolution ultrasound technique and drew blood to examine the concentration of ET-1,NO and the expression of ET-1 and eNOS mRNA before experiment and after three week’s therapy. The expanding percentage of the flow-mediated vasodilation(FMD) of brachial artery represented the endothelium-dependent vasodilatation(EDD) [EDD=(FMD-D0)/D0×100%]. Results Three groups had no significant difference in D 0, FMD and EDD of brachial artery before experiment. But the EDD of two therapeutic groups improved notably after three weeks’ therapy, and the Compound Salvia Miltiorrhiza Bunge Injection group was better than VitC group. There was no difference of ET-1 and NO among three groups before experiment. After three week’s therapy, the compound salvia miltiorrhiza bunge injection group showed decreasing in the concentration of ET-1 and expression of ET-1 mRNA,increasing in the concentration of NO and expression of eNOS mRNA, all that were significantly different from that of the control group(p<0.05). The VitC group also showed increasing in the concentration of NO and expression of eNOS mRNA, but lower than that of the Compound Salvia Miltiorrhiza Bunge Injection group(p<0.05). Conclusion The Compound Salvia Miltiorrhiza Bunge Injection could improve the brachial endothelial function of CHD patients by regulating the expressions of ET-1 and eNOS mRNA.

Abstract:Aim To evaluate the diagnostic value of serum lipids, lipoprotein (a) and their combination in coronary heart disease (CHD). Methods 546 patients with suspected CHD were enrolled into this study and divided into CHD group (n=354) and non-CHD group (n=192) according to the result of coronary arterography. Their clinical data were analysed by case-control method, and serum lipids were detected by standard method. Results Compared with non-CHD group, the levels of serum total cholesterol, low density lipoprotein cholesterol, lipoprotein (a) and the ratio of total cholesterol to high density lipoprotein cholesterol in CHD group were significantly raised, whereas the level of high density lipoprotein cholesterol were significantly lowered. There was no significant difference in serum triglyceride level and triglyceride/high density lipoprotein cholesterol ratio between two groups. The abnormal rate of total cholesterol, low density lipoprotein cholesterol, total cholesterol/high density lipoprotein cholesterol ratio and lipoprotein (a) in CHD group significantly increased, while the abnormal rate of other lipids didn't show significant difference. The predicative value and likelihood ratio of lipoprotein (a) for CHD was not superior to that of other lipids, but when combined with low density lipoprotein cholesterol, these value would further be elevated. In logistic regression model, lipoprotein (a) wasn't more related to CHD risk than other lipids. Conclusion The diagnostic value of lipoprotein (a) isn't better than other lipids. When combined with low density lipoprotein cholesterol, it may be regarded as a better predicative marker for CHD.

Abstract:Aim To discuss the curative effect and protection of Pracachol on carotid atherosclerosis. Methods 120 patients with carotid atherosclerosis and hyperlipaemia were randomly divided into treatment group and control group. The treatment group were treated with Pracachol 10 mg/d and their carotids and lipid level were checked after 3, 6 and 12 months in order to compare with the control group on the numbers and types of their carotid atheromatous plaques,carotid inner diameters (D), the thickness between carotid intima-media thickness (IMT). Results 3 months' treatment with Pracachol can decrease total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDLC) level in plasme efficiently, and as the treatment prolonged, the decrease of plaques'numbers, the change of plaques' type and the dinilution of IMT all has Statistcal significance. Conclusions Pracachol can decrease the lipid level in plasma efficiently, and to some extent, it can improve and stabilize the carotid atheromatous plaque as well.

Abstract:Aim To observe the regularity of fluctuation of serum C-reactive protein (CRP) level in patients with acute cerebral infarction (ACI) and to investigate the relationship between the serum CRP level and the development and prognosis of ACI, and its clinical significance. Methods The serum CRP level was determined serially (on day 1, 7 and 14 after onsets) by immune turbidity method in 66 patients with ACI and 45 normal controls. Results In ACI group, the serum CRP level increased on first day was significantly (p<0.01) higher than that in the controls, showing a highest serum CRP level in severe patients. It reached the peak on seventh day and then tended to decrease gradually. Conclusions This study suggests that high serum CRP level may play a role in the development of ACI, and serum CRP level is positivly correlated with severity extent of ACI.

Abstract:Aim To understand the effect of carvedilol on the coronary vascular endothelial function of the patients with coronary heart disease after percutaneous transluminal coronary angioplasty (PTCA). Methods 51 cases,having one or more than two branches narrow (≥70%),were diagnosed by coronary angiography. These patients were divided randomly into carvedilol group (n=28) and control group (n=23) who did not take carvedilol. Endothelin (ET) and nitric oxide (NO) levels of peripheral blood were measured before and after PTCA,before and after two week by taking carvedilol. Results Compared with the ET (carvedilol group: 70.6±12.8 μg/L,control group: 71.5±13.3 μg/L) and NO (carvedilol group: 50.3±13.4 μmol/L,control group: 50.9±12.6 μmol/L) levels before PTCA,ET (carvedilol group: 84.9±14.7 μg/L,control group: 85.6±15.4 μg/L) were markedly increased and NO (carvedilol group: 50.3±13.4 μmol/L,control group: 50.9±12.6 μmol/L) were decreased after PTCA (p<0.05); compared with the ET (84.4±14.9 μg/L) and NO (51.6±12.5 μmol/L) levels before taking carvedilol,ET (74.6±15.6 μg/L) were decreased and NO (62.7±12.8 μmol/L)were increased after two weeks (p<0.05),but the ET and NO levels of the control group did not change in the period of two-week observation (p>0.05). Conclusion Carvedilol may improve the coronary vascular endothelial function after PTCA.