Abstract:Aim To investigate the effects of ClC-3 antisense oligonucleotide on H2_O2-induced apoptosis in rat aortic vascular smooth muscle cells. Methods Western-blot was performed to detect the expression of ClC-3 protein. Morphological determination, DNA agarose gel electrophoresis, MTT assay and flow cytometry analysis were performed to measure the morphological changes, DNA ladder, viability and apoptotic rate and effects of ClC-3 antisense oligonucleotide on rat aortic smooth muscle cells. Results The antisense oligonucleotide specific to ClC-3 mRNA decreased the expression of ClC-3 protein and enhanced the apoptotic events induced by H₂O₂ including ultrastructural alteration and DNA ladder. The apoptotic cell death rate increased from 52.8%±13.6% to 75.7%±5.8% (n=6,p<0.01),and whereas the viability further decreased from 48.9%±4.3% to 31.3%±4.3 % (n=6,p<0.01) by ClC-3 antisense oligonucleotide transfection. Conclusion ClC-3 antisense oligonucleotide potentiated apoptosis induced by H₂O₂ in rat aortic smooth muscle cells.

Abstract:Aim To investigate the difference in the types and mechanisms of vascular remodeling among the different brain arteries. Methods The parameters of vascular remodeling and the smooth muscle cells (SMC)were measured through the HE staining photos of the arteries. Protein expression of fibronectin (FN) was determined by immunohistochemistry. Results The amount of SMC and FN expression level in carotid arteries decreased significantly while the SMC average area increased compared with SD at 4 weeks post-operation. At the end of eighth week, there was a significant increase in wall thickness, wall area, wall-to-lumen diameter ratio, wall-to-area ratio, SMC average area and FN expression level and a decrease in SMC amount of specific area of RHRSP carotid arteries. Wall area in RHRSP basial arteries had been increased since the fourth week post-operation and FN expression increased at the eighth week. There was a significant differece in lumen diamerer, wall-to-lumen diameter ratio and wall-to-area ratio between the middle cerebral arteries of SD and RHRSP (4 or 8 weeks post-operation). The wall thickness,wall area and the SMC amount of RHR middle cerebral arteries were significantly higher than SD at 8 weeks post-operation. Conclusions The difference in the types and mechanisms of vascular remodeling in RHRSP brain arteries may be connected with different stroke behavior among them.

Abstract:Aim To elucidate the change of intracellular reactive oxygen species (ROS) level and apoptosis in human umbilical vein endothelial cells (hUVEC and ECV304) after transfection with pcDNA3.1-nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) plasmid. Methods The level of NOX4 mRNA in hUVEC and ECV304 transfected with pcDNA3.1-NOX4 plasmid or pcDNA3.1-GFP plasmid was measured by RT-PCR. Intracellular ROS level and apoptosis rate were detected with flow cytometry. The apoptosis of hUVEC and ECV304 was observed by Hoechst staining and TUNEL staining. Results NOX4 mRNA expression and ROS level were increased significantly in hUVEC transfected with pcDNA3.1-NOX4 plasmid compared with control group and the group that were transfected with pcDNA3.1-GFP plasmid (p<0.05,n=3). NOX4 mRNA was also detectable in ECV304 transfected with pcDNA3.1-NOX4 plasmid, but not in control ECV304. The apoptosis rate were elevated significantly in hUVEC and ECV304 transfected with pcDNA3.1-NOX4 plasmid (the apoptosis rate of ECV304 and hUVEC is 9.6%±0.9% and 12.4%±1.1% respectively) compared with other two groups (the apoptosis rate of ECV304 and hUVEC in control group is 1.05±0.25%, 2.28±0.37% respectively, the apoptosis rate of ECV304 and hUVEC in the group that were transfected with pcDNA3.1-GFP plasmid is 1.56%±0.33% and 4.56%±0.62% respectively) as detected by flow cytometry (p<0.05, n=3). The results of Hoechst staining and TUNEL staining indicated that apoptotic cells present in hUVEC and ECV304 transfected with pcDNA3.1-NOX4 plasmid,but not in other two groups. Conclusion The transfection of plasmid pcDNA3.1-NOX4 results in over-expression of NOX4 in hUVEC and ECV304,inducing apoptosis of hUVEC and ECV304.

Abstract:Aim To test the hypothesis that exogenous administration of HIF1α could enhance the differentiation of endothelial progenitor cells (EPC) in hypoxia in vitro. Methods EPC were isolated from human peripheral blood by density gradient centrifugation. We transfected overexpressed HIF1αto EPC in normoxia/hypoxia by electroporation and measured the transfection effiency. HIF1α, HIF1β(ARNT), vascular endothelial growth factor (VEGF), nitric oxide (NO) level were measured with RT-PCR, Western blot, flow cytometry or Elisa. EPC morphology were also observed. Results Approximately 20% pEGFP+cells were observed after 36 h transfection. Compared with normoxia,the expression of both HIF1α mRNA and ARNT mRNA was not at all augmented in response to hypoxic stimulus (p<0.05). In contrast,VEGF mRNA expression was significantly up-regulated under hypoxia(p<0.05). HIF1α western bolt showed hypoxia stabilization of HIF1α protein was induced at 3 h, 6 h and 12 h in hypoxia while the expression of HIF1α protein was undetectable at 24 h in hypoxia. After 6-13 days cultured in 21% or 1% oxygen pressure, fluorescence-trace experiments revealed that CD31+EPC could be generated more effienciently from overexpressed HIF1α in hypoxia than that of pEGFP transfected EPC (p<0.05) (53.8%±3.7% vs 40.2%±4.3% under normoxia at d6; 66.2%±6.5% vs 51.8%±3.5% under normoxia at d13; 60.2%±5.0% vs 46.8%±3.5% under hypoxia at d6; 76.1%±1.9% vs 59.0%±3.5% under hypoxia at d13). A time kinetic NO was measured by Elisa Kit which was markedly enhanced by HIF1α in hypoxia (p<0.01). EPC differentiation was also observed by cell morphology. EPC differentiation and proliferation was more rapid in overexpressing of HIF1α group in hypoxia than in normoxia. Conclusions Hypoxia is ideal for EPC differentiation and proliferation. Overexpressing of HIF1α is important for exploring HIF1-dependent processes and for hypoxia-induced pathophysiological events. Moreover, HIF1α transfection was found to give a prospected way to do the insight research on ischemic treatment in vivo.

Abstract:Aim To observe the regulation of stromal derived factor 1(SDF-1) on monocytes-endothelial cells induced by low density lipoprotein (LDL). Methods LDL was separated by density gradient centrifugation. Reverse transcript-polymerase chain reaction (RT-PCR) and Western blot were separately used to detect the expression of mRNA and protein of SDF-1 in endothelial cells. Cell counting was used to observe the effect of the adhesion of monocytes/endothelial cells treated with LDL or SDF-1 antibody. Results Compared with the control group, the level of expression in LDL treated groups increased evidently as the LDL concentration increased. The adhered amount of monocytes to endothelial cells were 60±20, 97±26, 170±32, respectively responding to the LDL concentration 50 mg/L, 100 mg/L, 150 mg/L. And the amount was 20±5 in the control (p<0.01). While endothelial cells were incubated with SDF-1 antibody with 0.1 mg/L, 0.5 mg/L, 1 mg/L respectively before LDL incubation, the adhesion of monocytes was 113±23, 53±21, 41±10 respectively. They were significantly lower than that of control group (186±31) (p<0.05). Conclusion LDL increased the adhesion between monocytes and endothelial cells, which is closely correlative to the increasing expression of SDF-1 in endothelial cells.

Abstract:Aim To investigate the effects of nitric oxide (NO) in different concentration, nitric oxide synthase (NOS) activity and total antioxidative capability (T-AOC) in cardiac tissue, and the influence of isosorbide dinitrate (ISDN) in different dose after myocardial infarction (MI). Methods 32 New Zealand rabbits were randomly divided into four groups: sham-operated group, MI group, low dose of ISDN group (LISDN, 1.5 mg/kg·d), high dose of ISDN group (HISDN, 4.0 mg/kg·d), with the drugs gastric gavage three times everyday for six weeks. The NO concentration, all isoforms of NOS activity and T-AOC of cardiac tissue homogenate, adjacent to the infarcted area, were detected. The pathological changes were observed by microscope and electron microscope. Results The NO concentrations of MI group and HISDN group were higher than those of sham-operated group and LISDN group (0.980±0.180 μmol/g, 1.112±0.210 μmol/g, 0.497±0.129 μmol/g, 0.637±0.126 μmol/g, p<0.05 or 0.01). The inducible NOS (iNOS )activity in myocardial tissue of MI group and HISDN group was higher than that of sham-operated group and LISDN group (1 519±175 u/g, 1 659±175 u/g, 565±112 u/g, 852±106 u/g, p<0.01), while T-AOC was lower (856±183 u/g, 901±174 u/g, 1 654±207 u/g, 1 467±302 u/g,p<0.05). And constitutive NOS (cNOS) activity in myocardial tissue of MI group and HISDN group was lower than that of sham-operated group and LISDN group (1 034±301 u/g, 903±274 u/g, 1 615±227 u/g, 1 436±210 u/g, p<0.05). The injured pathological changes were light in sham-operated group and LISDN group. Conclusion High concentration of NO decreased the antioxidative capability of cardiomyocyte and led to injury after MI while low concentration of NO showed beneficial effects.

Abstract:Aim To investigate the effect of over-taking methionine on endothelial progenitor cells (EPC) in rabbit peripheral blood and the intervention of granulocyto-colony stimulating factor (G-CSF) in the process. Methods Newsland rabbits were divided into four groups: normal control, G-CSF, homocysteine (HCY), HCY+G-CSF groups. Normal and G-CSF groups were fed with normal food, HCY and HCY+G-CSF groups with 1% methionine food. The animals in G-CSF and HCY+G-CSF groups were injected with G-CSF 50 μg/d by belly cavity. EPC number in peripheral blood were surveyed at 1st, 2nd, 3rd, 4th, 8th, 12th week and serum nitric oxide (NO), HCY were also measured at 12th week. Results EPC in nomal control group had been low level basal line; EPC in G-CSF group had kept highest in the whole period; EPC in HCY group seemed descending at 1st, 2nd, 3rd, 4th week, and ascending at 8th, 12th week; EPC in HCY+G-CSF group decreased gradually, which was between that of G-CSF and normal control group. Compared with normal control group, EPC in HCY+G-CSF group was higher during the former two weeks. EPC in HCY+G-CSF group was lower than that in G-CSF group since 2nd week (p<0.01). At 12th week serum NO in HCY group was lower than that in HCY+G-CSF group (p<0.05), and serum NO were equal among normal control, G-CSF , and HCY+G-CSF groups. Serum HCY increased only in methionine food groups. Conclusion HCY reduced EPC in the beginning and hightened it later, descended serum NO which could been attenuated by G-CSF. G-CSF improved endothelium dysfunction caused by HCY, and the effect possibly related to mobilization of G-CSF to EPC.

Abstract:Aim To investigate the effects of peptide specific to CCR5 on monocyte chemotaxis. Methods The effects of peptide on the binding of mAb 2D7 to monocyte were surveyed by flow cytometry; Competitive binding of peptide and RANTES on monocyte was measured through Quantikine Human RANTES kit; Chemotaxis assay of monocyte toward peptide was performed in vitro;Effects of peptide on atherosclerosis formation was detected in vivo in mice. Results Peptide could inhibit the binding of 2D7 and RANTES to monocyte (IC50 was about 3.98 μmol/L). In vitro,peptide showed no chemotactic effect to monocyte(P=0.074) and could inhibit chemotactic activity of monocyte toward RANTES,the cell number of migration in the peptide+RANTES groups (23±10) was lower than that of the RANTES groups(62±13). Peptide could impair the influx of monocyte to the aortic root in mice(p<0.05). Conclusion Peptide could target to monocyte and suppress chemotactic activity of monocyte toward RANTES and reduce atherosclerosis.

Abstract:Aim To observe the effect of probucol on the neointimal hyperplasia and the expression of collagen type Ⅰand c-myc mRNA after coronary angioplasty in a swine model. Methods 19 female New Yorkshire pigs were randomly assigned to receive 2 g/d of probucol or control therapy for 4 weeks before percutaneous transluminal coronary angioplasty (PTCA), then PTCA was undergone in all the pigs, probucol was continued until follow-up angiography 6 weeks after PTCA. Then the animals were killed and taken histopathologic examination, the intima area ratio was measured. Immunohistochemical method was used to detect the expression of collagen type Ⅰin the injured arteries. Reverse transcription polymerase chain reaction (RT-PCR) method was used to detect the expression of c-myc mRNA in the injured arteries. Results The injured arteries in the control group revealed marked eccentric neointima formation, the intima area ratio was more than that in the probucol group (56.0%±17.8% vs 30.3%±21.0%, p<0.05). The expression of collagen type Ⅰin the probucol group was lower than that in the control group (0.22±0.06 vs 0.41±0.06, p<0.05). The expression of c-myc mRNA in the control group was higher than that in the normal artery (2.73 ± 0.51 vs 0.82±0.09, p<0.05), and the injured artery of the probucol group had lower expression of c-myc mRNA (1.44±0.25) than the control group (p<0.05), but had higher expression than the normal artery (p<0.05). Conclusions Probucol decreased the neointimal hyperplasia after PTCA, the mechanism may relate to inhibiting the expressions of collagen type Ⅰand c-myc mRNA in the injured artery.

Abstract:Aim To investigate the effects of soluble epoxide hydrolase inhibitor (sEHi) on cardiac hypertrophy. Methods The pathology changes of the hearts were observed in the pressure overload mice and pressure overload mice fed with sEHi. Semi-quantitative RT-PCR was used to measure the expression of hypertrophy genes: atrial natriuretic peptide (ANP), α-myosin heavy chain (α-MHC), β-myosin heavy chain (β-MHC), skeletal muscle alpha-actin (SM ɑ-actin). Western blot was used to measure the changes of nuclear factor (NF)-κB complex. Results sEHi could significantly decrease both heart weight/body weight ratio and dimension of left ventricular end systolic chamber, increase fractional shortening. It could also reduce hypertrophy gene expression, and inhibit the activity of NF-κB. Conclusion sEHi might inhibit pressure overload induced cardiac hypertrophy through the effects on NF-κB pathway.

Abstract:Aim To explore the role of advanced glycation end products (AGEs)in pathogenesis and development of diabetic complications, and analyse the immunological property of monoclonal antibodies (McAb)against AGEs. Methods Indirect ELISA and western blotting were used to analyse the immunological property of McAb and the epitope which would combine with McAb. AGEs in serum of human and aortas from diabetic rats were also detected by McAb. Results McAb reacted with AGEs specially and combined with non-carboxymethyl lysine (non-CML). AGEs in serum of human and aortas from diabetic rats had been detected, however, there had been no AGEs detected in aortas from normal rats. Conclusion McAb(non-CML)reacted with AGEs specially,and might be of value for AGEs measurement.

Abstract:Aim To evaluate the effects of atorvastatin on aortic blood pressure and ion pump activities of vascular smooth muscle cell in spontaneously hypertensive rats (SHR). Methods Twelve twelve -week-old SHR were randomized into atorvastatin treated group (ATV group, n=6)and distilled water group (DW group,n=6),and Wistar-Kyoto rats (WKY)as normal controls. Atorvastatin and appropriate amounts of distilled water were administered to ATV group for 12 weeks by gavage. Blood pressure of caudal artery was examined before and after treatment,serum titres of TC, TG, LDLC, activities of Na+-K+-ATPase and Ca 2+-Mg 2+-ATPase of thoracic aorta smooth muscle cell were measured. Results Blood pressure in ATV group was much lower than that in DW group(161.8±9.9 vs 192.9±10.4,p<0.05). Activities of Na+-K+-ATPase and Ca 2+-Mg 2+-ATPase of thoracic aorta smooth muscle cell were remarkedly higher in both ATV group and WKY group than those in DW group (5.20±0.54 vs 3.06±0.42,p<0.01;4.62±0.35 vs 2.98±0.17,p<0.05),(5.92±0.31 vs 3.06±0.42, p<0.01; 4.86±0.26 vs 2.98±0.17,p<0.01). Activities of Na+-K+-ATPase and Ca 2+-Mg 2+-ATPase of thoracic aorta smooth muscle cell were negatively relative to blood pressure(r=-0.426,r=-0.359,p<0.01). Conclusion Long-term administration of atorvastatin can effectively reduce blood pressure by elevating the ion pump activities of vascular smooth muscle cell.

Abstract:Aim To investigate the influence of all-trans retinoic acid (ATRA) on the process of luminal narrowing, the expression of some cell cycle modulatory factors in rats artery after aortic balloon withdrawal injury. Methods 54 SD rats were randomly divided into 3 groups. In control group (n=6) rats were killed at the 28th day after procedure. In operation group (n=24) and ATRA group (n=24) rats had balloon induced endothelium denudation at thoracic aorta and were killed at the 2nd, 7th, 14th, 28th day after artery injury. All rats were predosed with ATRA (30 mg/kg.d) or corn oil by gavage 4 days before injury and continued to each indicated time. After the thoracic aorta were harvested, we used immunohistochemistry staining to measure the protein expression of cyclin dependent kinase inhibitor P27 and proliferation cell nuclear antigen. Meanwhile vessel morphological measurement was taken. Results ①In normal rat arteries P27 was detected. After balloon injury, P27 expression in media decreased, reached the lowest level at the 2nd day and then upregulated while vascular smooth muscle cell (VSMC) reached peak proliferation at the 2nd day and then decreased quickly. In neointima, VSMC proliferated extremely at the 7th day, P27 could be detected at the 14th and 28th day when the proliferation of VSMC decreased. ②In ATRA-treated group P27 downregulation was inhibited in media, and P27 was already present in the neointima at the 7th day and strongly expressed at the 14 th and 28 th day while the proliferation of VSMC was significantly decreased (p<0.01). As a result ATRA group had a smaller noeintima /media area ratio, larger internal or external elastic lamina area and luminal area (p<0.01). ③The expression of P27 and the cell proliferation were in remarkable negative correlation (p<0.001). Conclusion The decreased expression of P27 may have an important role in the process of luminal narrowing after aortic balloon withdrawal injury.

Abstract:Aim To inquire into the relationship between single nucleotide polymorphisms (SNP) of thrombospondin-1 gene (TSP-1) and acute myocardial infarction (AMI). Methods Fragment of Exon thirteen in TSP-1 gene from 172 cases of AMI and 270 subjects without coronary heart disease were analysed by polymerase chain reaction and restriction fragment length polymorphism, and sequence analysis for confirmation. Results Of the 442 subjects participating in the study, only 6 of the heterozygotes and none of the homozygotes were detected for the 700S allele. No association of the N700S polymorphism with an altered risk of AMI was found in our study (GA vs AA: OR=3.19, 95%CI 0.578～17.61, P=0.160). Conclusion Our study suggested that the TSP-1 N700S polymorphism was rare and unrelated to AMI in the Chinese Han population. This study accumulated additional data on SNP in TSP-1 gene.

Abstract:Aim To explore the risk factors of atherosclerosis disease in the patients with type 2 diabetes mellitus. Methods Serum free fatty acid (FFA), total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDLC), high density lipoprotein cholesterol (HDLC), fasting blood glucose (FBG), glycosylated hemoglobin (HbA_1c), high sensitive C-reactive protein (Hs-CRP), tumor necrosis factor-α (TNF-α), fibrinogen (FIB) were tested in 170 type 2 diabetics and 74 non-diabetics as control group. These exposing factors and the incidence of atherosclerosis disease were compared in diabetic group and non-diabetic group by case control study. These exposing factors were compared in diabetics with atherosclerosis disease and without atherosclerosis disease and the risk factors of atherosclerosis disease were analyzed in statistic method. Results The incidence of atherosclerosis disease in type 2 diabetics was higher than that in control group (χ2=15.526, P=0.000, OR=3.088) and the confidence interval of 95% OR was 1.757～5.427. Multivariant Logistic regression analysis showed that the most important risk factor for atherosclerosis disease in type 2 diabetics was LDLC. The incidence of atherosclerosis disease in diabetics whose LDLC was higher than 2.6 mmol/L was 3 times that of whose LDLC was lower than 2.6 mmol/L (χ2=11.987, P=0.001, OR=3.073), and the confidence interval of 95% OR was 1.612～5.860. Conclusion The incidence of atherosclerosis disease in type 2 diabetics was 3 times that in non-diabetics. LDLC was the most important risk factor of atherosclerosis in type 2 diabetics.

Abstract:Aim To study the effect of percutaneous coronary intervention (PCI) on the activities of peripheral blood monocytes and inflammation in patients with stable angina pectoris (SAP). Methods 100 patients with SAP who underwent PCI or coronary angiography (CAG) were randomly divided into PCI group (n=48) and CAG group (n=52). Venous blood samples, from which peripheral blood monocytes were isolated by gradient centrifugation, were collected from all patients at 30 minutes before and 24 hours after PCI or CAG. Interleukin-1β (IL-1β), Interleukin-6 (IL-6), C-reactive protein (CRP), and serum amyloid A (SAA) in supernatant secreted by peripheral blood monocytes at baseline and after stimulation by lipopolysaccharide (LPS) were measured. Serum levels of infammatory biomarkers such as IL-1β, IL-6, CRP, and SAA were also measured and their relations to major adverse cardiovascular events (MACE) at a follow-up period of mean (8±3) months were analysed. Results Compared with those in CAG group, IL-1β (152.3±72.6 ng/L vs 99.4±60.2 ng/L, p<0.01), IL-6 (127.5±44.3 ng/L vs 65.6±36.5 ng/L, p<0.01), and SAA (102.8±54.4 μg/L vs 78.4±49.6 μg/L, p<0.05) in supernatant from peripheral blood monocytes at baseline increased significantly and increased further after lipopolysaccharide stimulation (p<0.01) in PCI group. Meanwhile, IL-1β, IL-6, and SAA secreted by peripheral blood monocytes correlated significantly with the corresponding serum levels respectively (p<0.05 or 0.01). In the follow-up period, although the rate of MACE was higher in the subgroup with higher infammatory biomarkers than that in subgroup with lower inflammatory biomarkers (37.0% vs 19.0%), the differences between them were nonsignificant statistically (p<0.05). Conclusions PCI increased the activities of peripheral blood monocytes and enhanced systemic inflammation in patients with SAP, which maybe associate with poor outcomes.

Abstract:Aim To explore the role of insulin resistance (IR)in atherosclerotic cerebral infarction (ACI)and lacunar cerebral infarction (LCI). Methods The serum concentrations of insulin after overnight fast and glucose load were determined by the use of radioimmunoassay and the serum concentrations of glucose, total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), lipoprotein (a) [Lp(a)], apolipoprotein A and B (ApoA, ApoB) after overnight fast and the serum concentrations of glucose after glucose load were measured by biochemical methods in 48 patients with ACI and 38 patients with LCI and 40 healthy control subjects. The plasmatic activities of tissue-type plasminogen activator (tPA)and plasminogen activator inhibitor-1 (PAI-1) were assayed by chromgenic substrate methods and levels of blood pressure and body mass index (BMI) was tested by routine ways in all subjects. Insulin sensitivity index (ISI) was estimated by the negative natural logarithm of the verse of fasting serum glucose and insulin product. Results The serum concentrations of glucose and insulin after overnight fast and glucose load (6.6±3.2 mmol/L and 6.3±2.3 mmol/L, 9.2±2.3 mmol/L and 9.2±2.5 mmol/L, 13.6±9.1 mIU/L and 13.4±8.0 mIU/L, 99.0±54.3 mIU/L and 98.4±53.9 mIU/L) were significantly higher in the two groups of cerebral infarction compared with the healthy control subjects (p<0.01), while the ISI (-4.20±0.24 and -4.19±1.02) in the two groups of cerebral infarction was significantly lower compared with the healthy control subjects (p<0.01). The increased levels of SBP(150.2±18.2 mmHg and 152.4±13.6 mmHg), DBP(96.2±12.7 mmHg and 97.4±18.6 mmHg), TG(1.71±0.68 mmol/L and 1.68±0.99 mmol/L), LDL(3.06±0.29 mmol/L and 3.01±0.40 mmol/L), TC(5.11±0.35 mmol/L and 4.98±0.34 mmol/L), Lp(a) (238±202 mg/L and 234±217 mg/L), PAI-1(880±350 AU/L and 870±150 AU/L) and BMI (26.5±1.1 kg/m2 and 26.3±2.0 kg/m2)were significantly observed in the two groups of cerebral infarction compared with the healthy control subjects (p<0.01), whereas decreased levels of HDL (1.24±0.48 mmol/L, 1.23±0.18 mmol/L)and tPA (0.28±0.16 kIU/L, 0.25±0.18 kIU/L) were detected significantly in the two groups of cerebral infarction compared with the healthy control subjects (p<0.01). The difference of all above parameters between two patients` groups had no statistical significance(p<0.05). In the patients with ACI and the patients with LCI, the ISI was negatively associated with the increased level of SBP, DBP, TG, ApoB, PAI-1 and BMI, but the ISI was positively associated with the decreased levels of HDL and ApoA, whereas the ISI was not associated with the levels of TC, LDL, Lp (a) and tPA. Conclusions IR which is the important risk factor in ACI and LCI plays an important part in both the atherosclerosis of large and medium cerebral arteries and the arteriosclerosis of small cerebral arteries.

Abstract:Aim To study the relationship between the occurrence of acute coronary syndrome (ACS) and hypercoagulable state. Methods Plasma prothrombin fragment 1 and 2 (F_ 1+2) and soluble fibrin monomer complex (SFMC) were detected by enzyme-linked immunosorbent assay for 86 patients with ACS and 75 patients with stable angina pectoris (SAP). Results Compared with SAP group, the plasma levels of F_ 1+2 and SFMC in ACS group were significantly higher (F_ 1+2: 1.21± 0.23 nmol/L vs 0.76±0.20 nmol/L, p<0.001; SFMC: 85.4±12.4 mg/L vs 68.7±13.8 mg/L,p<0.001). The plasma levels of F_ 1+2 and SFMC in ACS patients with diabetes mellitus were significantly higher than those in ACS patients who had no other diseases (F_ 1+2: 1.28±0.19 nmol/L vs 1.16±0.20 nmol/L, p<0.05; SFMC: 89.8±12.4 mg/L vs 82.7±13.7 mg/L,p<0.05). The plasma levels of F_ 1+2 and SFMC in ACS patients with essential hypertension were significantly higher than those in ACS patients who had no other diseases (F_ 1+2: 1.26±0.24 nmol/L vs 1.16±0.20 nmol/L, p<0.05; SFMC: 90.0±12.8 mg/L vs 82.7±13.7 mg/L, p<0.05). Conclusion Patients with SAP were in stable thrombotic state, patients with ACS were in unstable thrombotic state, the occurrence of ACS was closely related to hypercoagulable state.

Abstract:Aim There is a growing evidence showing that asymmetric dimethylarginine (ADMA) and intercellular adhesion molecule-1 (ICAM-1) are markers of endothelial dysfunction and the degree of coronary collateral circulation in subjects with severe coronary artery stenosis is attributed to endothelial injury. In the present study, we examined the serum levels of ADMA and ICAM-1 in patients with severe coronary artery stenosis and furthermore to investigate the correlation between the serum levels of ADMA and ICAM-1 with the degree of coronary collateral circulation. Methods 85 patients at least with the stenosis of one vessel >95% among three main vessels of coronary artery were consecutively enrolled in the study according to angiographic estimation in our hospital from June to November in 2005. Development of collaterals was classified by Rentrop's method. According to the collateral degree, patients were divided into two groups (poorly developed collateral group: 50 patients with grade 0 and 1; well-developed collateral group:35 patients with grade 2 and 3). The levels of ADMA and ICAM-1 were also determined. Results Compared with patients with poorly developed collateral group, the levels of ADMA of patients with well developed collateral group were significantly decreased (2.23±0.59 μmol/L vs 1.79±0.57 μmol/L, P=0.001). Similarly, the levels of ICAM-1 were also markedly reduced (272.4±68.3 μg/L vs 225.0±61.9 μg/L,P=0.002). Conclusions the present data suggest that poor collateral circulation is related to elevated levels of ADMA and ICAM-1 in patients with severe coronary artery stenosis.