自拟芪参通络汤对缺血性中风患者血管内皮功能的影响

目的观察自拟参芪通络汤对缺血性中风患者血管内皮功能的影响。方法将162例气虚血瘀兼水湿停滞证缺血性中风患者随机分为治疗组79例和对照组78例,对照组采用西医常规治疗,治疗组在此基础上给予自拟参芪通络汤口服,两组疗程均为14 d。结果治疗组治疗后内皮细胞依赖性舒张功能(FMD)及血管性假血友病因子(vWF)、非对称性二甲基精氨酸(ADMA)、内皮细胞钙黏蛋白(VE-Ca)等水平改善较对照组更加明显(P<0.05)。结论自拟芪参通络汤治疗缺血性中风,能够有效保护患者的血管内皮功能。

胎盘血管生成因子和子宫动脉多普勒检查定性不同类型的先兆子痫和孤立的胎儿宫内生长受限

Objective: The purpose of this study was to evaluate possible relationships between placental markers and endothelial dysfunction in preeclampsia and intrauterine growth restriction. Study design: A prospective study was conducted in 76 patients with preeclampsia and 37 patients with intrauterine growth restriction that were classified as early onset( < 34 weeks of gestational age) or late onset, and 40 control subjects. Plasma levels of placental growth factor, soluble fms-like tyrosine kinase-1, vascular cell adhesion molecule-1, and uterine artery Doppler indices were measured. Results: In early-onset preeclampsia and intrauterine growth restriction, placental growth factor was lower and soluble fms-like tyrosine kinase-1 and vascular cell adhesion molecule-1 higher than in control subjects, although all changes were more pronounced in preeclampsia. In late onset preeclampsia, those patients with abnormal uterine artery Doppler indices had higher soluble fms-like tyrosine kinase-1 and vascular cell adhesion molecule-1 levels. Conclusion: Biochemical changes in early-onset preeclampsia and intrauterine growth restriction point to a common placental disorder and a state of endothelial dysfunction, which may require interaction with other factors to explain the maternal disease in preeclampsia. Data in late-onset preeclampsia suggest that a proportion of them may occur with minimal placental involvement.

Associations of big endothelin-1 and C-reactive protein in atrial fibrillation

Background Atrial fibrillation （AF） is associated with inflammation and endothelial dysfunction. However, the association between inflammation （as indexed by high-sensitivity C-reactive protein, hs-CRP） and endothelial function [as indexed by big endothelin-1 （ET-1）] in AF patients remains unclear. Methods We enrolled 128 patients with lone AF, among which 83 had paroxysmal AF, and 45 had persistent AF. Eighty-two age- and gender-matched controls of paroxysmal supraventricular tachycardia without AF history were evaluated. Plasma hs-CRP, big ET-1 levels and other clinical characteristics were compared among the groups. Results Patients with persistent AF had higher hs-CRP concentrations than those with paroxysmal AF （P 〈 0.05）, both groups had higher hs-CRP level than controls （P 〈 0.05）. Patients with persistent AF had higher big ET-1 level than those with paroxysmal AF, although the difference did not reach the statistical significance （P 〉 0.05）, and both groups had higher big ET-1 levels than controls （P 〈 0.05）. Multiple regression analyses revealed hs-CRP as an inde- pendent determinant of AF （P 〈 0.001）. Further adjusted for big ET-1, both big ET-1 and hs-CRP were independent predictors for AF （P 〈 0.001）, but the odds ratio for hs-CRP in predicting AF attenuated from 8.043 to 3.241. There was a positive relation between hs-CRP level and big ET-1 level in paroxysmal AF patients （r = 0.563, P 〈 0.05）, however, the relationship in persistent AF patients was poor （r = 0.094, P 〈 0.05）. Conclusions Both plasma hs-CRP and big ET-1 levels are elevated in lone AF patients, and are associated with AF. In paroxysmal lone AF patients, there were significant positive correlations between plasma hs-CRP level and big ET- 1 level.

Androgen actions on endothelium functions and cardiovascular diseases

The roles of androgens on cardiovascular physiology and pathophysiology are controversial as both beneficial and detrimental effects have been reported. Although the reasons for this discrepancy are unclear, multiple factors such as genetic and epigenetic variation, sex-specificity, hormone interactions, drug preparation and route of administration may contribute. Recently, growing evidence suggests that androgens exhibit beneficial effects on cardiovascular function though the mechanism remains to be elucidated. Endothelial cells （ECs） which line the interior surface of blood vessels are distributed throughout the circulatory system, and play a crucial role in cardiovascular function. Endothelial progenitor cells （EPCs） are considered an indispensable element for the reconstitution and maintenance of an intact endothelial layer. Endothelial dysfunction is regarded as an initiating step in development of atherosclerosis and cardiovascular diseases. The modulation of endothelial functions by androgens through either genornic or nongenomic signal pathways is one possible mechanism by which androgens act on the cardiovascular system. Obtaining insight into the mechanisms by which androgens affect EC and EPC functions will allow us to determine whether androgens possess beneficial effects on the cardiovascular system. This in turn may be critical in the prevention and therapy of cardiovascular diseases. This article seeks to review recent progress in androgen regulation of endothelial function, the sex-specificity of androgen actions, and its clinical applications in the cardiovascular system.

Study on the Effect of Simvastatin on Left Ventricular Mass and Endothelial Function and the Relationship between Their Changes in the Patients with Essential Hypertension

Objective:To study the effect of Simvastatin on the left ventricular mass and endothelial function and to investigate the relationship between their changes in the patients with essential hypertension(EH). Methods: 50 patients with hypertension without severe complication were divided into two groups in a randomized,controlled and single blind trial.Group I(n=25)were given Simvastatin and hydragogue for 12 weeks while Group Ⅱ were given hydragogue during the same time.We detected the left ventricular mass and the brachial artery dilatation induced by reactive hyperemia(DIRH)or nitroglycerin(DING)respectively with ultrasonography in all patients before and after treatment.25 normal subjects without any treatment were taken as the control. Results:The left ventricular mass index(LVMI)was higher in the two groups of patients[(133.61±31.02)g/m 2;(118.04±39.62)g/m 2]than that in the control(88.79±22.73)g/m 2 before treatment(P<0.01,0.000 1,respectively)while the blood pressure was higher.The DIRH was lower in the two groups of patients(5.93±2.24)%;(6.54±3.16)%than that in the control(13.09±2.99)%,P<0.000 1.There was no significantly differences in age,serum concentrations of total cholesterol,triglyceride,sugar,blood pressure or the DING between two groups of patients and the control(P>0.05).And there was no significant difference in the all variables between group Ⅰ and group Ⅱ before treatment.After treatment the LVMI decreased[(133.61±31.02)g/m 2 VS(91.07±16.01)g/m 2,P<0.01]and the DTRH increased[(5.93±2.24)% VS(13.53±2.38)%,P<0.01]in the patients of group Ⅰ while there was no significant change in LVMI and DIRH in the patients of group Ⅱ.The blood pressure in the two groups of patients was decreased to the normal.Compared with group Ⅱ,the changes of LVMI and DIRH was higher in patients of group Ⅰ though the serum concentrations of total cholesterol,triglyceride or sugar were not significantly different.No significant change in serum concentrations oftotal cholesterol,triglyceride or sugar was found during treatment in the two groups of patients.Analysis showed that the LVMI correlated with DIRH and the change of LVMI correlated better with the change of DIRH(r=-0.56;0.69,P<0.000 1,respectly). Conclusions: The increase of left ventricular mass was related with endothelial dysfunction in essential hypertension.Being independent of the changes of serum concentrations of total cholesterol,triglyceride or sugar and blood pressure,Simvastatin could inhibit the increase of left ventricular mass and improve endothelial function.

Effects of Obstructive Sleep Apneas on Endothelial Function and Autonomic Modulation in Adult Man

Objective To study the effects of obstructive sleep apneas on endothelial function and autonomic modulation. Methods From June 2009 to June 2011, male patients with obstructive sleep apnea hypopnea syndrome (OSAHS) were consecutively enrolled in this study. Patients with an apnea/hypopnea index (AHI) of greater than 15 and without previous treatment for OSAHS were included as Group OSAHS and obese subjects with an AHI of less than 5 were included as non-OSAHS controls (Group Control). Electrocardiography and beat-to-beat blood pressure were continuously recorded from the radial artery by applanation tonometry which was synchronized with polysomnography recording. Endothelial function was measured by arterial augmentation index (AAI). Spectral analysis of heart rate variability (HRV) and blood pressure variability (BPV) were computed for cardiac parasympathetic modulation (high frequency power, HF); sympathetic modulation (low frequency power, LF), sympathovagal balance (LF/HF power of R-R variability, LF/HF) and BPV sympathetic modulation (BPV LF) in normalized units [total power of the components/(total power-very LF power)×100]. Results Finally, 27 moderate-severe OSAHS patients and 22 non-OSAHS obese controls were recruited in the Group OSAHS and Group Control, respectively. In Group OSAHS, the age was 43.3±9.3 year-old, body mass index (BMI) was 36.8±8.7 kg/m 2 ; in Group Control, the age was 42.9±8.6 year-old, BMI was 34.4±7.9 kg/m 2 ; there were no significant differences in age and BMI between the Group OSAHS and Group Control (all P>0.05). The baseline AAI (12.5%±2.2% vs. 8.2%±2.1%) and BPV LF (68.3%±13.5% vs. 61.1%±11.7%) of the Group OSAHS were significantly higher than those of the Group Control (all P<0.05). And after overnight sleep, systolic BP (143.7±14.2 vs. 132.8±13.3 mm Hg), diastolic BP (87.7±7.7 vs. 78.6±5.5 mm Hg), HRV LF (69.7%±14.4% vs. 64.3%±12.1%), HRV LF/HF (3.7±2.0 vs. 2.3±1.3) and BPV LF (77.8%±15.6% vs. 68.3%±13.5%) of the Group OSAHS were significantly increased (all P<0.001), while HRV HF was significantly decreased (21.1%±9.3% vs. 27.5%±10.3%, P<0.05) from baseline.Conclusions The baseline endothelial function and autonomic modulation are impaired in OSAHS patients, which happened prior to hypertension and other cardiovascular complications. And the load effects of overnight obstructive breathing events could induce blood pressure and sympathetic activity increasing in the morning in OSAHS patients without acute aggravation in endothelial dysfunction.

Hypertension in the elderly： insights from recent research

Hypertension is a leading cause of mortality and morbidity around the world and,prevalence of hypertension is increasing with aging.Hypertension in the elderly is associated with increased occurrence rates of sodium sensitivity,isolated systolic hypertension,and ＇white coat effect＇.Arterial stiffness and endothelial dysfunction also increase with age.These factors should be considered in selecting antihypertensive therapy.The prime objective of this therapy is to prevent stroke.The fmdings of controlled trials show that there should be no cut-off age for treatment.A holistic program for controlling cardiovascular risks should be fully discussed with the patient,including evaluation to exclude underlying causes of secondary hypertension,and implementation of lifestyle measures.The choice of antihypertensive drug therapy is influenced by concomitant disease and previous medication history,but will typically include a thiazide diuretic as the first-line agent;to this will be added an angiotensin inhibitor and/or a calcium channel blocker.Beta blockers are not generally recommended,in part because they do not combat the effects of increased arterial stiffness.The hypertension-hypoten-sion syndrome requires case-specific management.Drug-resistant hypertension is important to differentiate from faulty compliance with medication.Patients resistant to the third-line drug therapy may benefit from treatment with extended-release isosorbide mononitrate.A trial of spironolactone may also be worthwhile.

A Decreased Responsiveness of Platelet to Nitric Oxide in Cholesterol-Fed Rabbits

Objective:To determine whether endothelial dysfunction leads to an abnormal responsiveness of platelet to nitric oxide(NO)during the development of atherosclerosis. Methods:Rabbits were fed a 1% cholesterol chow for 12 weeks to induce atherosclerosis.Serum NOx levels and the responsiveness of platelet to NO donor SNP were determined every 4 weeks during maintaining on a chow containing 1% cholesterol.The measurement of serum lipids and the examination of morphological feature and endothelial-dependent relaxation of aorta were performed after 12 weeks of cholesterol diet. Results:Cholesterol diet significantly increased serum levels of cholesterol and LDL,caused a remarkable platelet hyperaggregability,and produced an evident endothelial dysfunction as indicated by the diminished vasorelaxation induced by acetylcholine and endothelial cell lesion as exhibited by scanning electron microscope examination.The percentage of inhibition of ADP-induced platelet aggregation by NO donor SNP was significantly smaller in cholesterol chow group than that in normal chow group although no significant difference in serum NOx levels between normal and cholesterol chow group was observed throughout the development of atherosclerosis. Conclusion:The present study suggests that the endothelial dysfunction caused by enhanced serum cholesterol and LDL levels induces a decreased responsiveness of platelet to NO.

Recombinant vascular basement-membrane-derived multifunctional peptide inhibits angiogenesis and growth of hepatocellular carcinoma

AIM： To investigate the anti-angiogenic and antitumor activities of recombinant vascular basement membrane-derived multifunctional peptide （rVBMDMP） in hepatocellular carcinoma （HCC）. METHODS： HepG2, Bel-7402, Hep-3B, HUVE-12 and L-02 cell lines were cultured in vitro and the inhibitory effect of rVBMDMP on proliferation of cells was detected by MTT assay. The in vivo antitumor efficacy of rVBMDMP on HCC was assessed by HepG2 xenografts in nude mice. Distribution of rVBMDMP, mechanism by which the growth of HepG2 xenografts is inhibited, and microvessel area were observed by proliferating cell nuclear antigen （PCNA） and CD31 immunohistochemistry. RESULTS： MTT assay showed that rVBMDMP markedly inhibited the proliferation of human HCC （HepG2, Bel-7402, Hep-3B） cells and human umbilical vein endothelial （HUVE-12） cells in a dose-dependent manner, with little effect on the growth of L-02 cells. When the ICs0 was 4.68, 7.65, 8.96, 11.65 and 64.82 μmol/L, respectively, the potency of rVBMDMP to HepG2 cells was similar to 5-fluorouracil （5-FU） with an IC50 of 4.59 μmol/L. The selective index of cytotoxicity to HepG2 cells of rVBMDMP was 13.8 （64.82/4.68）, which was higher than that of 5-FU [SI was 1.9 （8.94/4.59）]. The VEGF-targeted recombinant humanized monoclonal antibody bevacizumab （100 mg/L） did not affect the proliferation of HepG2, Bel-7402, Hep-3B and L-02 cells, but the growth inhibitory rate of bevacizumab （100 mg/L） to HUVE-12 cells was 87.6% ± 8.2%. AIternis diebus intraperitoneal injection of rVBMDMP suppressed the growth of HepG2 xenografts in a dose-dependent manner, rVBMDMP （1, 3, 10 mg/kg） decreased the tumor weight by 12.6%, 55.9% and 79.7%, respectively, compared with the vehicle control. Immunohistochemical staining of rVBMDMP showed that the positive area rates （2.2% ± 0.73%, 4.5%± 1.3% and 11.5% ±3.8%） in rVBMDMP treated group （1, 3, 10 mg/kg） were significantly higher than that （0.13% ± 0.04%） in the control group （P 〈 0.01）. The positive area rates （19.0% ± 5.7%, 12.2% ± 3.5% and 5.2% ±1.6% ） of PCNA in rVBMDMP treated group （1, 3, 10 mg/kg） were significantly lower than that （29.5% ± 9.4%） in the control group （P 〈 0.05）. rVBMDMP at doses of 1, 3 and 10 mg/kg significantly reduced the tumor microvessel area levels （0.26%± 0.07%, 0.12% ± 0.03% and 0.05% ± 0.01% vs 0.45% ± 0.15%） in HepG2 xenografts （P 〈 0.01）, as assessed by CD31 staining. CONCLUSION： rVBMDMP has effective and unique anti-tumor properties, and is a promising candidate for the development of anti-tumor drugs.

THE LONG TERM EFFECT OF CAPTOPRIL TREATMENT ON ENDOTHELIAL FUNCTION IN SPONTANEOUSLY HYPERTENSIVE RATS

The aim of this study is to elucidate the long term effect Of captopril treatment on the endothelial func-tion to release nitric Oxide (NO) in spontaneOusly hypertensive rats (SHR). The properties of endotheliumwere determined with a model of hindquarter perfusion in response to al adrenergic agonist, phenylephrine,at the age of 40 weeks of SHR which was administrated with captopril (100 mg/kg/day) from lntrauterineand withdrawn at 16 weeks of age. Furthermore, in the presence of N-nitro-L-arginine methyl ester(LNAME), or L-arginine, the responses to phenylephrine were studied. From the curve of perfusion pres-sure, the minimal, maximal perfusiOn pressure (PPmin,PPmax) and the maximal slOpe (slope),as well asthe 5O% of effective concentratiOn (EC,,) were obtained. The data show that in captopril treated SHR,PPmin, PPmax and slope were markedly lower, but EC50 higher than those of untreated SHR. The curveinduced by phenylephrine was significantly right shift compared with that of untreated SHR. Like WKY,the intensive reactivity to phenylephrine in the presence of LNAME was much lower than that of untreatedSHR. ln the presence of L-arginine, however, the right shift of curves was seen only in captopril treatedSHR and WKY rats, but not in control SHR. In conclusipn, endothelium does involve in the respnse ofresistant vessel to phenylephrine. The mechanism of enhanced reactivity In untreated SHR may be, at leastin part, due to the diminished capacity of producing No frpm endpthelium, and the effect pf sustained hy-potension of early captopril treatment might be relevant to the improved ability of endOthelium.

Effect of Liandouqingmai Recipe on life quality and vascular endothelial injury in patients with coronary heart disease

OBJECTIVE:To observe the effects of Liandouqingmai Recipe on life quality and vascular endothelial injury in patients with coronary heart disease.METHODS:Capitalized 101 patients with coronary heart disease were randomly divided into a treatment group(n=45) treated with Liandouqingmai Recipe and a standard treatment group(control group,n=56).A normal group of 16 healthy persons was additionally set up.Changes in ET-1 and NO levels were measured and Seatle Angina Questionnaire(SAQ) was adopted in studying life quality before and after treatment for two weeks.The data were analyzed with SPSS 16.0 statistic software.RESULTS:The average level of ET-1 in the normal group was lower and NO higher than that of patients with coronary heart disease.There was no significant difference in the average level of ET-1 and NO and in the scores of SAQ [physical limitation(PL),pngina stability(AS),apngina frequency(AF),treatment satisfaction(TS) and disease perception(DP)] between the two groups before treatment(P>0.05).But after treatment,the scores of SAQ(PL,AS,AF,TS,DP) and NO level were higher than those in the control group,and ET-1 average level in the treatment group was lower than that in the control group.The negative relations between PL and ET-1 and between AF and ET-1 were found in this study.CONCLUSION:Liandouqingmai Recipe can raise scores of SAQ and NO level and decline ET level in patients with coronary heart disease on the basis of convertional standard treatment,thus improving vascular endothelial function and life quality.Life quality is related to vascular endothelial function.

Effects of Liandou Qingmai Recipe(连豆清脉方) on Endothelin-1,Nitric Oxide,Interleukin-6 and Interleukin-10 Levels in Patients with Coronary Heart Disease

Objective:To observe effects of Liandou Qingmai Recipe(连豆清脉方) on endothelin-1(ET-1),nitric oxide(NO),interleukin-6(IL-6) and IL-10 levels in patients with coronary heart disease.Methods:Total 101 cases with coronary heart disease were randomly divided into a treatment group(n=45) treated by Liandou Qingmai Recipe and a standard treatment group(control group,n=56),with a normal group of 16 health persons set up.Changes of ET-1,NO,IL-6 and IL-10 levels were measured before treatment and after treatment for two weeks.And the data were analyzed by SPSS 16.0 statistic software.Results:Before treatment,the levels of ET-1,IL-6 and IL-10 levels were significantly higher and NO was significantly lower in the patients with coronary heart disease than those in the normal group(90.7±12.7 ng/L vs 41.8±13.5 ng/L,9.17±0.18 ng/L vs 1.10±0.08 ng/L,1.94±0.26 ng/L vs 1.09±0.06 ng/L,and 92.2±17.7 μmol/L vs 124.5±27.2 μmol/L;all P<0.05),with no significant differences in the levels of ET-1,NO,IL-6 and IL-10 between the treatment group and the control group(P>0.05);After treatment,ET-1 and IL-6 significantly decreased in the treatment group and the control group,and NO increased in the treatment group;And IL-6 level was significantly lower and NO level was higher in the treatment group than those in the control group(4.48±1.22 ng/L vs 5.13±1.85 ng/L,117.4±22.3 μmol/L vs 92.4±17.1 μmol/L;both P<0.05);There was a positive correlation between IL-6 and IL-10,and a negative correlation between NO and IL-10(r=0.142,r=-0.152;both P<0.05).Conclusion:Liandou Qingmai Recipe can decline IL-6,IL-10 and ET-1 levels,and raise NO level in patients with coronary heart disease on the basis of standard treatment,so as to inhibit endothelial inflammatory response,improve vascular endothelial function,with stronger anti-AS action;And vascular endothelial lesion is related with inflammatory response.

Influence of moxibustion temperatures on blood lipids, endothelin-1, and nitric oxide in hyperlipidemia patients

OBJECTIVE： To observe the influence of moxibustion temperature on blood lipids, endothelin-1（ET-1）, nitric oxide（NO）, and ET-1/NO in hyperlipidemia patients. METHODS： Forty-two primary hyperlipidemia patients were randomly divided into two groups of 21 and treated with moxibustion at different temperatures. Moxibustion was performed with the moxa roll 2.5-3.0 cm from the skin in the treatment group and 4 cm in the control group, 10 min per point, once every other day. Skin temperature was precisely measured with a thermometer during moxibustion. After a 12-week treatment, seven measurements of blood lipids, ET-1, and NO were recorded. RESULTS： Total cholesterol and triglyceride, were lower in the treatment group than in the control group（P0.05）. Serum ET-1 and ET-1/NO was obvi-ously lowered in the treatment group（P0.001）. Moxibustion regulated NO and ET-1/NO in the treatment group much better than in the control group. CONCLUSION： Moxibustion can regulate blood lipids and clear blood vessels. Moxibustion at 45℃has a better effect than moxibustion at 38℃ on regulating blood lipids and protecting vascular endothelial function, indicating that suitable temperature influences the curative effect of moxibustion.

Pitavastatin calcium improves endothelial function and delays the progress of atherosclerosis in patients with hypercholesterolemia

Background： Statins have proven efficacy in inhibiting the onset and progress of atherosclerosis. The effectiveness of pitavastatin in reversing carotid atherosclerosis associated with hypercholesterolemia （HC） is un-known. Objectives： To explore the simultaneous effects of pitavastatin calcium on brachial arterial flow-mediated vasodilatation （FMD）, carotid intima-media thickness （IMT）, and arterial stiffness （β）, three surrogate markers of ath-erosclerosis were studied in HC patients. Methods：A randomized, double-blind trial was performed with 40 HC sub-jects who fulfil ed the inclusion/exclusion criteria. Patients were given pitavastatin calcium 1 mg/d （Group 1） or 2 mg/d （Group 2） for 8 weeks. There were 20 patients in each group, and 30 gender-and age-matched healthy subjects as controls were recruited. FMD of the brachial artery, carotid IMT, and arterial stiffness indicated byβwere measured at baseline and at 8 weeks after starting pitavastatin calcium therapy using ultrasound techniques. Biochemical tests were also made on al subjects. Results： At baseline, higher total cholesterol （TC） and low-density lipoprotein cho-lesterol （LDL-C）, reduced FMD, and increasedβand IMT were observed in HC patients （P0.05）. Significant negative interactions between TC/LDL and FMD （P〈0.05–0.001）, positive interactions between TC and IMT （P=0.003） and between TC/LDL and β （P〈0.001–0.000） were found. Conclusions： Treatment with pitavastatin calcium exerted fa-vorable effects on endothelial function and arterial stiffness. It also improved carotid atherosclerosis in patients with HC.

Enhanced External Counterpulsation Inducing Arterial Hemodynamic Variations and Its Chronic Effect on Endothelial Function

To make clear the precise hemodynamic mechanism underlying the anti-atherogenesis benefit of enhanced external couterpulsation(EECP) treatment, and to investigate the proper role of some important hemodynamic factors during the atherosclerotic progress, a comprehensive study combining long-term animal experiment and numerical solving was conducted in this paper. An experimentally induced hypercholesterolemic porcine model was developed and the chronic EECP intervention was subjected. Basic hemodynamic measurement was performed in vivo, as well as the arterial endothelial samples were extracted for physiological examination. Meanwhile, a numerical model was introduced to solve the complex hemodynamic factors such as WSS and OSI. The results show that EECP treatment resulted in significant increase of the instant levels of arterial WSS, blood pressure, and OSI. During EECP treatment, the instant OSI level of the common carotid arteries over cardiac cycles raised to a mean value of 8.58 ×10-2±2.13 ×10-2. Meanwhile, the chronic intervention of EECP treatment significantly reduced the atherosclerotic lesions in abdominal aortas and the endothelial cellular adherence. The present study suggests that the unique blood flow pattern induced by EECP treatment and the augmentation of WSS level in cardiac cycles may be the most important hemodynamic mechanism that contribute to its anti-atherogenesis effect. And as one of the indices that cause great concern in current hemodynamic study, OSI may not play a key role during the initiation of atherosclerosis.

Post-transcriptional gene regulation by RNA-binding proteins in vascular endothelial dysfunction

Endothelial cell dysfunction is a term which implies the dysregulation of normal endothelial cell functions,including impairment of the barrier functions,control of vascular tone,disturbance of proliferative and migratory capacity of endothelial cells,as well as control of leukocyte trafficking.Endothelial dysfunction is an early step in vascular inflammatory diseases such as atherosclerosis,diabetic vascular complications,sepsis-induced or severe virus infection-induced organ injuries.The expressions of inflammatory cytokines and vascular adhesion molecules induced by various stimuli,such as modified lipids,smoking,advanced glycation end products and bacteria toxin,significantly contribute to the development of endothelial dysfunction.The transcriptional regulation of inflammatory cytokines and vascular adhesion molecules has been well-studied.However,the regulation of those gene expressions at post-transcriptional level is emerging.RNA-binding proteins have emerged as critical regulators of gene expression acting predominantly at the post-transcriptional level in microRNA-dependent or independent manners.This review summarizes the latest insights into the roles of RNA-binding proteins in controlling vascular endothelial cell functions and their contribution to the pathogenesis of vascular inflammatory diseases.

The effect of cigarette smoke extract on thrombomodulinthrombin binding: an atomic force microscopy study

Cigarette smoking is a well-known risk factor for cardiovascular disease. Smoking can cause vascular endothelial dysfunction and consequently trigger haemostatic activation and thrombosis. However, the mechanism of how smoking promotes thrombosis is not fully understood. Thrombosis is associated with the imbalance of the coagulant system due to endothelial dysfunction. As a vital anticoagulation cofactor, thrombomodulin (TM) located on the endothelial cell surface is able to regulate intravascular coagulation by binding to thrombin, and the binding results in thrombosis inhibition. This work focused on the effects of cigarette smoke extract (CSE) on TM-thrombin binding by atomic force microscopy (AFM) based single-molecule force spectroscopy. The results from both in vitro and live-cell experiments indicated that CSE could notably reduce the binding probability of TM and thrombin. This study provided a new approach and new evidence for studying the mechanism of thrombosis triggered by cigarette smoking.

Barrier stabilizing mediators in regulation of microvascular endothelial permeability

Increase of microvascular permeability is one of the most important pathological events in the pathogenesis of trauma and burn injury. Massive leakage of fluid from vascular space leads to lose of blood plasma and decrease of effective circulatory blood volume, result- ing in formation of severe tissue edema, hypotension or even shock, especially in severe burn injury. Fluid resusci- tation has been the only valid approach to sustain patient＇s blood volume for a long time, due to the lack of overall and profound understanding of the mechanisms of vascular hyperpermeability response. There is an emerging concept in recent years that some so-called barrier stabilizing media- tors play a positive role in preventing the increase ofvascu-lar permeability. These mediators may be released in re- sponse to proinflammatory mediators and serve to restore endothelial barrier function. Some of these stabilizing mediators are important even in quiescent state because they preserve basal vascular permeability at low levels. This review introduces some of these mediators and reveals their underlying signaling mechanisms during endothelial barrier enhancing process.