Abstract:Cholesterol efflux from lipid-loaded cells is a key event associating with stability and subsidence of plaque. There are many proteins and factors participating in regulation of cholesterol efflux of lipid-loaded cells, which is very complex. We propose,by summarizing the recent research,a novel mode of “four systems and one center with coupling transportation and networking regulation". The novel mode consists of 1) intracellular trafficking system of caveolin-1 complex,2) transmembrane transporting system of ATP binding cassette transporter(ABC)-A1 complex,3) transmembrane transporting system of scavenger receptor (SR-) B1 complex,4) extracelluar trafficking system of high density lipoprotein/apolipoprotein (HDL/Apo)-A1 and 5) caveolae transporting center. In brief,caveolin-1 complex system transports cholesterol from intracellular compartments to caveolae; both ABC-A1 and SR-B1 complex systems transfer cholesterol from caveolae to HDL/Apo-A1. There are networking regulation among four systems. This mode provides a simple and concise way to understand the dynamic process of atherosclerosis.

Abstract:Aim To investigate the effect of human vascular endothelial growth factor 165 (hVEGF165) cDNA mediated by recombinant adeno-associated viral vector2 (rAAV-2) on the angiogenesis in ischemic myocardium. Methods Rabbit myocardial ischemic models were generated by ligation of the anterior descending coronary artery. All these models were randomly divided into 4 groups: VEGF high dose group (10 12v.g./kg), VEGF middle dose group (10 11v.g./kg), VEGF low dose group (10 10v.g./kg) and control group. RAAV-2/hVEGF165 or PBS was injected into the ischemic myocardium respectively. After 4 weeks, the expression of objective gene was evaluated by RT-PCR and ELISA. The histological changes of myocardium were observed through histological sections. Myocardial capillary counts were calculated to evaluate the proangiogenic effects. Results With the increasing dosage of injected rAAV-2/hVEGF165, hVEGF165/GAPDH mRNA ratio were 0.14±0.03, 0.40±0.04 and 0.64±0.04 respectively, while VEGF protein content were 64.6±8.0 ng/L, 327.1±9.9 ng/L and 471.6±6.9 ng/L respectively. The changes of expression were dose-dependent and there were significant difference among the groups(p<0.01). In rAAV-2/hVEGF165 10 10, 10 11 and 10 12 v.g./kg treatmented groups, the microvessel counts were (4.6±1.3)/HPF, (11.6±1.8)/HPF and (21.8±3.1)/HPF respectively, while (4.5±1.5)/HPF in control group. There was significant difference between the 10 11, 10 12 v.g./kg hVEGF165 gene-treated groups and control group(both p<0.01), but no such difference between 10 10 v.g./kg hVEGF165 gene-treated group and control group(p>0.05). The result of correlation analysis showed the microvessel counts were related with the dosages of rAAV-2/hVEGF165 positively (r=0.910,p<0.01). Conclusions hVEGF165 gene mediated by rAAV-2 can be efficiently transferred into rabbit ischemic heart and induce angiogenesis of myocard-

Abstract:Aim To explore the effect of Li Shui Tiao Zhi capsule (LSTZ) on mitogen-activated protein kinases signal of vascular smooth muscle cells induced by mildly oxidized low density lipoprotein. Methods Serum-containing LSTZ was produced by general serum pharmacology assay method and protein was removed by methanol. LDL was oxidized by incubation with Cu 2+. c-Jun N-terminal kinase (JNK1), extracellular signal regulated kinase (ERK1/2) phosphorylation was examined by Western Blot assay. Results 20% serum-containing LSTZ significantly reduced the phosphorylated JNK1 level, but ERK1 and ERK2 phosphorylation level after mm-LDL-stimulation was not altered significantly. Conclusions The preferential reduction of the activation of the JNK/SAPK signal transduction pathway might be one of the mechanisms for inhibition of VSMC proliferation caused by LSTZ.

Abstract:Aim To explore the response and depressor of calcitonin gene-related peptide (CGRP) in the early phase of the 2-kindney, 1-clip Goldblatt hypertensive rats (2K1C), and the changes of treatment with perindopril or prazosin in this phase. Methods The 2K1C hypertensive rats were developed by part clipping the left renal artery. The plasma concentration of angiotensin Ⅱ and CGRP were determined by radioimmunoassay. CGRP mRNA expression was determined by reverse-transcription polymerase chain reaction (RT-PCR). Results The level of CGRP in plasma significantly increased compared with control groups (p<0.01). Perindopril significantly decreased the blood pressure concomitantly with an increase in the plasma concentration of CGRP and the expression of CGRP mRNA in dorsal root ganglia (DRG) in the 2K1C Goldblatt rats. Prazosin caused a hypotensive effect compared with 2K1C rats. Conclusions These results suggest that the 2K1C Goldblatt model exhibits a compensatory increase of sensory nerve actions, and that the depressor effects of perindopril may be related to stimulation of the synthesis and release of CGRP in the 2K1C Goldblatt hypertensive rats.

Abstract:Aim To explore the effect of fenofibrate on oxidized low density lipoprotein (ox-LDL) uptake in adipocytes from hypercholesterolemia rabbits and the expression of CD36. Methods 10 male New Zealand white rabbits were fed with 1% cholesterol, 7.5% protein, 8% lard diet for 8 weeks, and were randomly divided into two groups: ① high cholesterol group: maintained cholesterol diet for 4 weeks; ② treatment group: the same cholesterol diet supplemented with fenofibrate (30 mg/kg/day) for 4 weeks. And control group was fed with normal diet for 12 weeks. Subcutaneous adipose tissues were collected for adipocytes culture. CD36 and PPARγ mRNA expression were evaluated by RT-PCR. Results The specific cell association and degradation of 125 Ⅰ ox-LDL in adipocytes from the three groups exhibited a dose-dependent saturation pattern. The endocytic uptake and degradation of 125 Ⅰ ox-LDL in adipocytes from high-cholesterol groups were inhibited; fenofibrate treatment enhanced the 125 Ⅰ ox-LDL uptake and degradation in adipocytes from hypercholesterolemia rabbits. There were obviously difference among the three groups (p<0.05). The expression of PPARγ and CD36 mRNA in adipocytes were down-regulated in high cholesterol group and the CD36 mRNA expression in adipocytes of treatment group was similar to the control group. Conclusion Fenofibrate treatment improved the ox-LDL uptake and degradation in adipocytes from hypercholesterolemia rabbits and up-regulated CD36 mRNA expression in adipocytes.

Abstract:Aim We employed rat vascular calcific model induced by vitamin D 3 intramuscular injection and oral nicotine, and rat calcific vascular smooth muscular cells (VSMC) induced by β-glycerophosphate to study the possible mechanism which was involved in the regulatory action of ghrelin in vascular calcification. Methods The total aorta Ca content in aorta and VSMC were measured by atom absorptive spectrophotography; the alkaline phosphatase (ALP) activity were determined by the use of phenyl diphosphate-2-sodium; aortic 45 Ca-deposition was detected with the using of 45 CaCl 2; the mRNA expression of ghrelin, osteopontin (OPN) and endothelin were analyzed by reverse-transcript PCR, and the levels of ghrelin in plasma, endothelin in plasma and aorta were determined by radioimmunoassay. Results Vitamin D 3 and nicotine induced vascular calcification in rats and β-glycerophosphate induced calcification in VSMC too. The calcification in aorta was significantly attenuated by subcutaneous administration with ghrelin 30 and 300 nmol/kg for 4 weeks, and the latter dosage was more potent than the former. After the ghrelin treatment, the total aorta Ca 2+ contents, aortic 45 Ca-deposition, ALP activity were less respectively, than those in the rats with vascular calcification, but the OPN mRNA was up-expressed. After treated with ghrelin 10 -8～10 -6 mol/L, the calcification in VSMC was also attenuated, with decrease in the total Ca 2+ content, 45 Ca-deposition and ALP activity in VSMC in a concentration-dependent manner, so did the increase in OPN mRNA expression. In addition, we observed that endothelin levels of plasma and aorta and aortic endothelin mRNA expression significantly increased in the rats with vascular calcification, and ghrelin treatment significantly decreased them, with high dosage more portent than the lower. Conclusion Our results indicated that ghrelin can significantly attenuate the calcification in aorta and VSMC partly through the antagonism with endothelin system in circulation and vascular tissues.

Abstract:Aim To investigate the effect of fibroblast growth factor 2 (FGF2) cDNA mediated by recombinant adeno-associated viral vector2 (rAAV-2) on ischemic myocardium. Methods 20 rabbit myocardial ischemic models were generated by ligation of the anterior descending coronary artery. All these models were randomly divided into 2 groups: FGF2 gene therapy group (1012 v.g./kg) and control group. RAAV-2/FGF2 or PBS was injected into the ischemic myocardium respectively. After 4 weeks, the expression of objective gene mRNA was evaluated by RT-PCR. The histological changes of myocardium and other organs were observed through histological sections. Myocardial capillary counts were calculated to evaluate the proangiogenic effects. Results FGF2 gene expression was observed in rAAV-2/FGF2 treatment group. The microvessel counts of this group and control group were (12.0±1.4)/HPF and (4.5±1.5)/HPF respectively. There was significant difference between two groups(p<0.01). In rAAV-2/FGF2 1012 v.g./kg treatment group, there was no FGF2 gene expression in liver, kidney, spleen, cornea or testis. And no abnormality was detected in tissues structure through histopathological detection. Conclusions FGF2 gene mediated by rAAV-2 can be efficiently transferred into rabbit ischemic heart and induce angiogenesis of myocardium successfully. FGF2 gene expression is limited in myocardium.

Abstract:Aim To furnish evidence of the protective barrier formed by the edge-flowing blood in vessels within cerebral cortex. Methods The corrosion casts of the microvasculature of cerebral cortex were studied by scanning electron microscopy on ten dead China children’s heads perfused with methylemthacrylate to discover the shape of endothelium of the microvessel within cerebral cortex. The characteristics of microvessel cerebral cortex were studied with microscope on 18 sides children’s cerebral hemisphere perfused with the mixture liquid of formaldehyde (formalin) and carbon black ink,the proportion was 1:6. Confocal laser scanning microscopy was used in a rabbit opening cranial window preparation in order to study optical section on the microcirculation within the cerebral cortex in vivo. The plasma was labeled by fluorescein in capillaries was visualized up to 300 μm beneath the rabbit brain surface in noninvasive optical sections. The diameter of capillaries and the thickness of edge-flowing blood in vessels were measured. The gray scale display of axial blood flow and edge-blood flow in varying vessels was measured by image analytical system, and drew a curve of gray scale display. The normal microcirculation within cerebral cortex of rabbit, the microcirculation within cerebral cortex of normal rabbit treated with the Ligustrazine (or Tetramethylpyrazine) for moving the vessel, the microcirculation within cerebral cortex of shock rabbit treated with the Ligustrazine for moving the vessel was studied by Confocal laser scanning microscopy in vivid. Results There are four kinds of microvessel within the cerebral cortex, including the superficial, middle, deep cortical artery and cortical-medullar artery. The shape of endothelium of the microvessel within the cerebral cortex in children is crude, and it’s morphology is similar to the bark of poplar or willow and pine tree. The endothelium of blood vessels within cerebral cortex in human change from roughness to smoothness as the internal diameter of the blood vessels change from large to small. Under the normal state in vivid, the edge-flowing blood in vessels within cerebral cortex was stable when the diameter of capiuaries was 121.56 μm (P=0.0262) and 60.00 μm (P=0.0539) respectirely under the shock state, the edge-flowing blovd was stable when the diameter was 60.15 μm (P=0.9358) and 48.84 μm (P=0.0053) respectinely. Conclusions There is a protective barrier formed by the edge-flowing blood in vessels within cerebral cortex, which can cover and protect the endothelium of vessels within cerebral cortex, and avoid the cerebraovascular disease.

Abstract:Aim To establish insulin resistant hypertensive rat model and investigate the effects of insulin resistance and serum leptin level on serum lipids. Methods Male Spraque-Darley rats were fed on high fructose diet and the levels of blood pressure, serum insulin, leptin, triglyceride, total cholesterol and high density lipoprotein cholesterol were measured. The HOMA model was used to evaluate insulin resistance. The relationships between each parameters were analyzed. Results At the end of 8 weeks,in high fructose fed rats, blood pressure, serum insulin level and insulin resistance were significantly higher than those in control group, following hyperleptinemia and dislipidemia. In high fructose-fed rats, insulin resistance was positively related to blood pressure, serum leptin and triglyceride, while negatively to high-density lipoprotein-cholesterol. Also serum leptin was positively related to blood pressure, serum insulin,triglyceride and insulin resistance. Conclusions High fructose diet can induce insulin resistance, hypertension, hyperleptinemia and dislipidemia in male Spraque-Darley rats. Insulin resistance and leptin have a wide influence on lipids metabolism.

Abstract:Aim To investigate the effect of sodium ferulate(SF), one of the principal components of rhizoma ligustici wallichii, on the migration induced by endothelin-1 (ET-1) and platelet derived growth factor (PDGF) in vascular smooth muscle cells(VSMC). Methods Cultured VSMC derived from spontaneously hypertensive rats(SHR) were used. Cell migration was determined by modified Boyden chamber assays. [Ca 2+]i was measured with fluorescent Ca 2+ indicator Fura-2/AM. Results ET-1 and PDGF significantly induced a migration of VSMC in a dose-dependent manner, which was inhibited by pre-treatment of VSMC with SF(10 -7～10 -3mol/L) dose-dependently. The peak inhibition rate of migration induced by ET-1 and PDGF were 85.04% and 81.92% (p<0.01) respectively. ET-1 and PDGF provoked the rise of [Ca 2+]i in VSMC which was significantly suppressed by 10 -3 mol/L SF(p<0.01)with a inhibitory peak at 80.14% and 76.69%. Conclusions The migration and rise of [Ca 2+]i induced by ET-1 and PDGF in VSMC from SHR may be suppressed by SF.

Abstract:Aim To investigate the relationship of tumor necrosis factor-α(TNF-α),matrix metalloproteinases(MMPs) and NF-κB on postmyocardial infarction progressive heart failure in rats. Methods Male rats were randomised to proximal left anterior descending branch coronary artery ligation. The rats were killed on weeks 4, 8, and 12 after ligation to examine hemodynamic parameters. Protein expression of TNF-α, MMPs gelatinlytic activity and NF-κB activity was assessed from noninfarcted myocardium, sham-operated rats were used as the control group. Results Compared with sham-operated group, the myocardial infarction rats showed significant decrease in mean arterial pressure(MAP), maximal ascending and descending velocity of the left ventricular pressure(±dp/d tmax) and significant increased in left ventricular end-diastolic pressure(LVEDP) (all p<0.05). In comparison with sham-operated group, TNF-α production was increased significantly, MMP-2 and MMP-9 zymographic activity, NF-κB activity, and collagen volume fraction(CVF) increased significantly at weeks 4, 8 and 12 after ligation in noninfarcted myocardium. Conclusions TNF-α overexpression is related to increase in MMP gelatinlytic activity and NF-κB activity, which suggests that TNF-α can play an important role in postinfarction ventricular remodeling and progressive heart failure.

Abstract:Aim To investigate the effects of Losartan on expression of mitogen-activated protein kinases (MAPK) and vessel proliferation in a rabbit model of early accelerated atherosclerosis. Methods Aortic cholesterol content, expression of proliferation cell nuclear antigen (PCNA) and MAPK protein were detected by enzymatic analysis and immunohistochemistry. Results The ratio of vascular intimal to medial thickness, numbers of positive PCNA cells, and expression of MAPK protein in As group singnificantly increased compared with control group. There was a significant decrease in the ratio of vascular intimal to medial thickness, numbers of positive PCNA cells and expression of MAPK protein (p<0.001) in the Losartan-pretreated group. Aortic cholesterol content in the Losartan-pretreated group was significantly decreased compared with As group (p<0.05). Conclusion Losartan inhibits vascular MAPK expression, intimal proliferation and decreases cholesterol deposit in vascular walls which may play an important role in prevention of atherosclerosis.

Abstract:Aim To investigate the inhibitory effect of Cilostazol on matrix metalloproteinase-2 (MMP-2) and MMP-9 and tissue metalloproteinase inhibitor-1 (TIMP-1)and TIMP-2 protein and mRNA expression, to study its role and mechanism on proliferation after angioplasty. Methods 40 Japanese male white rabbits were injuried two times to make PTA models and divided into three groups: control group, high cholesterol group and Cilostazol group. PTA was proceeded under X-Ray, 4 weeks after the angioplasty, the damaged segments of abdominal arteries were harvested for morphometry (assessing NIA, MA, CA)and for immunohistochemical analysis as well as RT-PCR to evaluate MMP-2, MMP-9 and TIMP-1, TIMP-2 protein and mRNA expression level. Results Cilostazol can reduce the NIA and increase the CA. MMP-2, MMP-9 and TIMP-1, TIMP-2 protein and mRNA expression levels in high cholesterol control group increases at 4 th week after angioplasty. However, Cilostazol can reduce their levels. Conclusions Cilostazol can inhibit the vascular intimal hyperplasia, through its effect on the expression of MMP and TIMP to regulate the extracellular matrix turnover.

Abstract:Aim To investigate the effect of ACEI and ARB on the transcription factor NF-κB activation in monocytes induced by lipopolysaccharide (LPS). Methods Monocytes from normal deliveried female umbilical veins were incubated with bacterial LPS in presence or absence of different ACE inhibitors or angiotensin Ⅱ AT1 antagonists. At the end of incubation,the cells were harvested by trypsin digestion method. In order to evaluate a possible contribution of ACEI and ARB on NF-κB activation induced by LPS, we used western blotting to study phosphorylation and degradation of inhibitor protein IκBαin the cytoplasmic,the translocation of p65 subunits to the nucleus at different times. Results The data showed that LPS-dependent phosphorylation and degradation of IκBα was markedly impaired in ACEI and ARB-treated monocytes and the translocation of p65 subunit to the nucleus was inhibited at the same time. Conclusions ACEI and ARB has inhibitory effect on the transcription NF-κB activation in monocytes.

Abstract:Aim To study the effects of 4-hydroxy-2-nonenal (HNE) on cultured human aortic endothelial cells so as to explore the mechanism of the pathogenesis of atherosclerosis. Methods In single cell gel electrophoresis, quantitative DNA damage detection was used to identify the DNA damage at different concentrations in cultured human aortic endothelial cells. Results Tail moment was 32.8±1.1, 44.3±1.0 and 74.6±1.0 when human aortic endothelial cells were treated with 5 μmol/L, 10 μmol/L and 15 μmol/L of HNE for 10 hours, which were of statistical significance when compared with the normal group (6.0±0.7, p<0.001 respectively), but when human aortic endothelial cells was treated with 1 μmol/L of HNE, the tail moment was 11.3±0.9, which was of no statistical difference compared with the untreated group(p>0.05). Conclusion HNE induces DNA damage of cultured aortic endothelial cells. The DNA damage levels are proportional to the HNE concentrations.

Abstract:Aim To observe the effect of anti-oxidizer's improving vascular endothelial function on the early damage of the kidney in hypertension patients. Methods 120 subjects were randomly divided into pressure-lowering control group and anti-oxidizing treating group. Ultralente-nifedipine and probucol in addition to ultralente-nifedipine together were respectively given to the two groups for 12 weeks, and the changes of blood lipoprotein, endothelins(ET), β 2-MG in blood and urine and Alb in urine before treatment with those after treatment. Results First, there were the damage of endothelial function and the early damage of the kidney. Second, there was obvious decrease in ET-1, low-density cholesterol, β 2-MG in blood and urine and Alb in urine after treatment, and the difference was significant (p<0.05); while the above indexes decreased more remarkably in the anti-oxidizing treating group (p<0.01). Conclusions Anti-oxidizing treating can improve vascular endothelial function and diverse the early damage of the kidney in the hypertension patients better than only pressure-lowering treatment. It was pointed out that endothelins damage possibly had some association with the damage of the kidney in the hypertension patients.

Abstract:Aim To investigate the relationship between tumor necrosis factor-β gene polymorphism as well as its serum levels and coronary heart disease. Methods Nested polymerase chain reaction (PCR) coupled with allele-specific PCR (AS-PCR) were used for the detection of tumor necrosis factor-β genotype in 290 elderly patients with coronary heart disease and 239 elderly healthy controls. The serum tumor necrosis factor-β levels were measured by ELISA. Results Three genotypes CC, CA, AA were detected in both groups, and the genotypes were 25.9% and 37.2%, 49.3% and 45.6%, 24.8% and 17.2%, patients and controls respectively. There were statistically significant differences in the distributions of the genotypes (p<0.05) and the allele frequencies (p<0.05) between two groups. The relative risk suffered from coronary heart disease of AA and CA genotypes was 1.701 times of the CC genotype (Or=1.701, 95%CI: 1.173～2.466). The serum tumor necrosis factor-β levels of the patients were significantly different from that of the controls (p<0.05), however, among different tumor necrosis factor-β genotypes (CC, CA, AA) of patients and controls respectively, there were no significantly differences. Conclusions The single nucleotide polymorphism (SNP) at position 804 in the exon 3 of tumor necrosis factor-β gene is associated with coronary heart disease and the allele A may be a risk factor for coronary heart disease in Chinese. tumor necrosis factor-β gene polymorphism may affect coronary heart disease through its serum levels.

Abstract:Aim To investigate the effect of reperfusion therapy on plasma brain natriuretic peptide (BNP) levels and left ventricular remodeling (LVRM) in patients with acute myocardial infarction (AMI). Methods The study group included 56 patients with acute myocardial infarction (AMI), 38 patients undergone successful early reperfusion therapy as the reperfusion group, 18 patients undergone non-successful or rejected reperfusion therapy as the non-reperfusion group. Peripheral blood samples were taken at admission, on 24 hours, 48 hours, day 7, day 14, and day 28 after admission for BNP measurement by ELISA. The indexes of LVRM include left ventricular end diastolic volume index (LVEDVI), left ventricular end systolic volume index (LVESVI) and left ventricular eject fraction (LVEF) were measured by ultrasonic cardiogram on day 3～5 and day 28. △LVEDVI, △LVESVI and △LVEF were obtained by subtracting values of day 3～5 from which of day 28. Results Plasma BNP levels in patients with AMI were higher than those in health. In reperfusion group only one peak of BNP values was detected on 24 hours after admission, but two peaks of BNP values were detected in non-reperfusion group, the first peak on 24 hours and secondary peak on day 7 after admission. The reperfusion therapy can attenuate the enlarge of LVEDVI, LVESVI and improve LVEF. Conclusion The reperfusion therapy can decrease BNP levels , attenuate LVRM and improve LVEF.

Abstract:Aim To investigate the association of activated coagulation factor Ⅶ (FⅦa) and its gene MspI polymorphism for cerebral infarction with hypertension in Chinese. Methods This study was performed with the method of candidate gene and case-control study. FⅦ genotypes were identified with polymerase chain reaction amplified genomic deoxyribonulieic acid (DNA) and MspI restriction fragment length polymorphism analysis,and plasma FⅦa levels were detected with recombinant tissue factor method in 149 hypertensive patients, 132 hypertensive patients with ischemic stroke (stroke group) and and 148 normotensive sex- and age- matched control subjects. Results Plasma FⅦa levels were significantly higher in patients with ischemic stroke than those of patients with hypertension (2.78±0.59 v.s 2.53±0.62 μg/L, p<0.05). FⅦa is a risk factor for ischemic stroke with hypertension on Logistic regression analysis.(Or=1.134, p<0.05). The allelic frequencies were in Hardy-Weinberg equilibrium. The results suggested that the distribution of genotype and allelic frequencies in every group had no significant difference, also no difference in subgroups of ischemic stroke (p>0.05). FⅦa levels were significantly higher in Arg homozygotes than in Gln allele carriers (2.72±0.60 v.s 1.98±0.59 μg/L, p<0.05)and associated with FⅦ gene polymorphism. Conclusions Plasma FⅦa levels may be an important risk factor of cerebral infarction with hypertension and the levels are influenced by MspI polymorphism of the FⅦ gene.

Abstract:Aim To observe the expression of cyclooxygenase-2 (COX-2) mRNA in peripheral blood monocytes from patients with acute coronary syndrome (ACS), and the effects of atorvastatin on it. Methods Expression of COX-2 mRNA in peripheral blood monocytes from 18 normal control subjects and 42 patients with acute coronary syndrome were analyzed by reverse transcription -polymerase chain reaction (RT-PCR), and the monocytes from patients had been incubated with atorvastatin (0～10 μmol/L)in vitro. Results Expression of COX-2 mRNA significantly increased in peripheral blood monocytes from the patients with ACS compared with those from normal control subjects (1.64±0.25 vs 0.59±0.21, p<0.05). Atorvastatin significantly reduced the expression of COX-2 mRNA in peripheral blood monocytes from patients with ACS (p<0.05), and the reduction is relative to the concentration of atorvastatin. Conclusions These findings suggest that COX-2 may play an important role on the inflammation in atherosclerosis. Atorvastatin may have anti-inflammatory effects which are related to its effect on COX-2.

Abstract:Aim To investigate the association between von Willebrand factor (vWF) and the numbers of coronary artery stenotic lesions in acute coronary syndrome. Methods The concentration of plasma vWF was measured by enzyme linked immuoserbent assay (ELISA) in 54 patients with acute coronary syndrome and 15 stable angina pectoris and 20 normal persons without any angiographically detectable coronary artery disease. The relationship between plasma vWF level and the number of coronary vessels with stenosis was assessed. Results The concentrations of plasma vWF in patients with acute coronary syndrome were significantly higher than those in patients with stable angina pectoris (p<0.05) or control subjects (p<0.05). The level of plasma vWF was obviously higher in the multiple-vessel groups than in the single-vessel group (p<0.05), and the concentration of plasma vWF was positively related to number of vessels with percent stenosis of >50% diameter (r=0.224, p<0.05). Conclusions The vWF level, which is an indicator of thrombogenesis and endothelial damage, was significantly increased in patients with acute coronary syndrome. It is an indicator of distinguishing and predicting acute coronary instability and it is influenced by the degree of coronary atherosclerosis.

Abstract:Aim To investigate the vulnerable mechanism of mildly lesion by analyzing the structural characteristics of plaque. Methods In 62 patients with angiographic mildly coronary stenosis (diameter stenosis 20%～60%) and 26 patients with several stenosis, intravascular ultrasound (IVUS) imaging was performed. The characteristics of the atherosclerosis plaques were analyzed and stenosis rate was calculated. Results Compared with patients with angiographic several stenosis, patients with angiographic mildly lesion had more soft plaque (68.2% vs 15.4%, p<0.01), thin fibrosis cap (65.9% vs 7.7%, p< 0.01), plaque rupture ( 28.2% vs7.7%, p<0.01), and positive remodeling (51.8% vs 0%, p<0.01). Patients with mildly lesion had more eccentric plaques (84.7% vs 30.1%, p<0.01) and less calcification (16.5% vs 84.6%, p<0.01) than those with angiographic several stenosis. Conclusions In the majority of angiographic mildly coronary stenosis, plaques have several structural features of vulnerability. These features may be contributed to acute coronary syndrome.

Abstract:Aim To investigate the relationship between platelet and cerebral infarction as well as carotid atherosclerosis. Methods Positive rates of PAC-1 and CD62P,which are both platelet membrane glycoproteins,were measured by flow cytometry in blood samples while carotid artery were evaluated by color Doppler ultrasound in 75 patients with atherosclerotic cerebral infarction and 61 healthy examination persons. Results Positive rates of PAC-1 and CD62P in the cerebral infarction groups no matter with or without carotid atherosclerosis were significantly higher than that in the corresponding control groups. In addition,the positive rates in the groups with carotid atherosclerosis were significantly higher than those in the groups without carotid atherosclerosis both in cerebal infarction groups and in control groups. Farthermore,the positive rates in the groups of cerebral infarction with carotid atherosclerosis were the highest. Conclusion The level of platelet activation is associated with cerebral infarction and carotid atherosclerosis. Activating platelet may play an important role in atherosclerotic cerebral infarction.

Abstract:Aim To measure the activity of nuclear factor-κB (NF-κB) of the peripheral blood mononucleus cells (PBMC) of patient which had acute coronary syndrome (ACS) or stable angina or hypertension, study its relationship with C-reactive protein (CRP), plaque stability and determine its value in the diagnosis of ACS. Methods We compared the results of the activity of nuclear factor-κB and levels of CRP in ACS aged 48-80 years with that of the stable angina (SA) or hypertension as controls. Results OD of NF-κB p50 of PBMC and CRP in ACS group on admission was significantly higher than that in SA group and hypertension group (p<0.01), OD of NF-κB p50 of PBMC and CRP in AMI group on admission was significantly higher than that in UA group (p<0.05). OD of NF-κB p50 of PBMC and CRP in SA group had no difference from that in hypertension group. After two weeks, OD of NF-κB p50 of PBMC in ACS group was significantly decreased compared with that on admission (p<0.01). There was no difference between SA group and hypertension group. There was a positive correlation between OD of NF-κB p50 of PBMC and blood glucose level (r=0.512, p<0.01) in ACS group. OD of NF-κB p50 of PBMC also had a positive correlation with serum CRP level(r=0.771, p<0.01). Conclusions The activation of NF-κB in peripheral blood mononucleus cells may be a predictor of the coronary plaque instability and disruption, and it might be helpful in the diagnosis of ACS.

Abstract:Aim To compare multiple ECG testing measurements with coronary angiography and study the diagnostic ability of ST segment horizon tal elongation on the coronary stenosis severity. Methods CAG and ECG were performed in 334 cases respectively. Results Sensitivity of diagnosing CAG of ST segment horizontal elongtion (≥0.12 s) is superior to ST segment depression and ischemic T waves. In mild, moderate and severe CAD cases, the comparison of the sensitivity is as follows:51%vs41%,38%; 75%vs 52%,56%(p<0.01);100% vs 96%, 100%(p>0.05). Moreover,comparison between ST segment horizontal elongation (≥0.12 s) and CAG demonstrated: When the stenosis is less than 90% in both single and multiple coronary arteries disease, the positive rate is 47%,68%; When the stenosis is more than 90% in both single and multiple coronary arteries disease, the positive rate is 73%,100%.(p<0.01) The difference is significant between them. Conclusion The prolongation of ST segment may not only serve as one of marks for the diagnosis of early CAD because of its higher sensitivity but also be used for the anglysis of the severity of coronary stenosis because of its important values to detect severe CAD.

Abstract:Aim To discuss the relationship of abnormal distribution of Ca 2+ and formation of 26 Binswager’s disease, and to find how to prevent the disease. Method Binswager group and control group were detected by flow cytometry. Results IECa 2+ in blood hemocytes was significantly higher in encephalatrophy group than that in control group (p<0.05). In the group with severe cerebral atrophy manifested by computer tomography, IECa 2+ was higher than that of mild and moderate cerebral atrophy group. In the group with dementia, which were detected by the score of intelligent determination, the increase of IECa 2+ was much more remarkable than that of control group and prophase dementia group (p<0.05). Conclusions The formation mechanism of Binswager’s disease was related to abnormal distribution of IECa 2+. The abnormal distribution of IECa 2+ may activate cross-linking of cellular endogenic ribozyme and antibody of T lymphocyte, evoke neurotransmitter release in synapses, change the deformation ability of erythrocyte and aggregation function of platelet, thereby aggravate ischemia of cerebral tissues. Calcium antagonists can prevent Binswager’s disease caused by cerebral circulation disorder.

Abstract:Aim To evaluate the relationship between 5A/6A polymorphism in the promoter of stromelysin-1 gene and cerebral thrombosis in Chinese population. Methods The stromelysin-1 promoter 5A/6A polymorphism in 1 122 patients with cerebral thrombosis and 1 123 controls were screened by polymerase chain reaction (PCR), and then corresponding probe hybridization was performed. Results The distribution of 5A/6A polymorphism was in agreement with Hardy-Weinberg Equilibrium in both patients and controls. The prevalence of 5A5A, 5A6A and 6A6A genotypes were 2.50%, 27.63% and 69.88% in patients, and 2.23%, 26.18% 71.59% in controls, respectively. No significant difference was observed between these two groups (p>0.05). The 5A allele frequencies were 16.31% in patients, and 15.32% in controls. There is no dramatic distinction between cases and controls, either (p>0.05). Conclusion 5A/6A polymorphism in the promoter of stromelysin-1 gene is not a genetic marker of cerebral thrombosis in Chinese population.

Abstract:Aim Except high density lipoprotein cholesterol(HDLC), all the atherogenic lipoprotein cholesterol [including Iow density lipoprotein cholesterol (LDLC), cholesterol of lipoprotein riched triglycerides(TG) and lipoprotein (a) cholesterol] are included in the non-HDLC, which can be used in prediction of the atherogenic cardio vascular risk and as secondary target of lipid lowering therapy. The non-HDLC level can be simply estimated by subtract HDLC from total cholesterol(TC). This study was to provide the reference values and its distribution of serum non-HDLC data of Beijing populations. Methods 28 161 Beijing institutional employees (including those retired, but physical workers were excluded), male/female 6∶4, aged 20～85 years were enrolled in this study. All the subjects participated regular physical examination and well standardized lipid analysis with fasting blood samples (including TC, HDLC and TG. LDLC was calculated by Friedewald formula). Results Non-HDLC levels elevated gradually with increase in age. Male groups had higher average non-HDLC than female groups before age 50, but it was reversed due to much more increase in non-HDLC levels in women after age 50. Age adjusted mean non-HDLC were 3.47 mmol/L in men and 3.29 mmol/L in women. However, in the elderly men and women, the corresponding mean levels were 3.90 and 4.21 mmol/L respectively. It was supposed that the cutoff point of normal TG is 1.7 mmol/L, then the non-HDLC should be 0.77 mmol/L higher then LDLC at that point. But the TG level of most subjects in this study were lower then 1.7 mmol/L, the differences in the level between non-HDLC and LDLC were more or less lower then 0.77 mmol/L in different age groups, the non-HDLC level in this study was 20% lower than the report of Third National Health and Nutrition Examination Survey of US. It indicates that the atherogenic cardiovascular risk is much lower in the subjects of this studied group. Conclusion In the case of higher TG levels (>2.3 mmol/L), non-HDLC will better represent the concentrations of all atherogenics lipoproteins then LDLC alone. The method of non-HDLC estimation is simple and accurate.

Abstract:Aim To elucidate the effects of percutanious coronary intervention (PCI)on QT dispersion (QTd)and to find out its clinical significance. Methods The electrocardiograms recorded before and one day after PCI in 138 patients with acute myocardial infarction (AMI)were analyzed. The duration from the onset of AMI to PCI operation was less than 6 h in 72 patients and 6 to 12 h in others. All the patients underwent emergent and subsequently coronary stenting. QT intervals, QTd, and heart-rate-corrected QT intervals (QTc) and QTd (QTcd)were gauged and calculated. Results In both the less-than- and the longer-than-6-hour group, QT and QTc after PCI were not significantly different from before PCI. But the QTd and the QTcd after PCI were remarkably decreased(all p<0.01). Moreover, the QTd and QTcd in the less-than-6 h group were significantly shorter than those in the longer-than-6 h group (all p<0.05). And the inhospital mortality was 4.2% and 7.6%,respectively (P=0.394). Conclusions Successful PCI could notably reduce QTd in patients with AMI. The earlier the PCI was performed,the better the effects of reperfusion by PCI on reducing QTd.

Abstract:Aim To study the values of color doppler ultrasonography (CDU) for vertebral artery cervical spondylosis. Methods The changes of structure, velocity (V), blood flow volume (Q), resistance index (RI), and pulsatility index (PI) of 50 cases were studied. 30 healthy subjects were included in the study and served as a control group. Results As compared with the control group, RI and PI were significantly increased (p<0.05) and systolic peak flow velocity (SPV), end-diastolic flow velocity (EDV), Q were slightly reduced(p>0.05) in cervical spondylosis group(p>0.05). Conclusions CDU provide a valuable objective basis on morphological and hemodynamic changes of the vertebral artery cervical spondylosis patients with vertebrobasilar insufficiency (VBI).

Abstract:Aim To develop a method of culturing vascular smooth muscle cells (VSMC) from isolated rat thoracic aorta and compare their growth with that of aortic VSMC by other culture method. Methods The vascular media of rat thoracic aorta was isolated from male Wistar rats in sterile condition. Mince the media, and suspend the media in 10 mL 0.25% trypsin for about 3.5 h at 37℃. After terminating the digestion, centrifuge the solution at 100 g for 5 min, and seed the cell into a 25 cm2 vented cap flask. Results Thoracic aorta smooth muscle cell (SMC) were successfully passaged more than 20 times, without noticeable changes in morphology, growth characteristics, and smooth muscle α-actin expression. Conclusions Compared with the currently employed methods, our technique has the advantages of good reproducibility, high yield of pure SMC and quick growth of primary culture.