老年阻塞性睡眠呼吸暂停低通气综合征患者血管内皮舒张功能的变化

目的 评价老年阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血管内皮舒张功能的变化.方法 老年中重度OSAHS患者30例及对照组28例,分别测定血浆一氧化氮(NO)含量;用高分辨率超声检测基础状态、反应性充血时(内皮依赖性血管扩张)及含服硝酸甘油后(非内皮依赖性血管扩张)的肱动脉内径,计算不同状态下肱动脉的扩张率以评估血管内皮功能.老年中重度OSAHS患者经过4周经鼻持续气道内正压通气(nCPAP)治疗后重复多导睡眠监测、血浆NO含量和血管内皮功能测定.结果 老年中重度OSAHS组的血浆NO含量[(50.35±8.65)gmol/Li较对照组[(57.31±9.31)μmol/Li降低(t=2.95,P=0.005),接受4周的nCPAP治疗后血浆NO含量[(55.77±8.87)μmol/Li有明显升高(t=2.40,P=0.02).老年中重度OSAHS组反应性充血时肱动脉内径扩张率[(9.78±4.82)%较对照组[(13.21±5.81)%]明显减低(t=2.45,P=0.017);而对照组和老年中重度OSAHS组由硝酸甘油介导的血管扩张率分别为(16.87±6.15)%和(14.74±5.82)%(t=1.36,P=0.18).老年中重度OSAHS组接受4周nCPAP治疗后反应性充血时肱动脉内径扩张率为(14.33±6.13)%,较治疗前明显改善(t=3.20,P=0.002),而硝酸甘油介导的血管扩张率为(15.15±4.21)%,较治疗前无明显变化(t=0.31,P=0.76).结论 老年中重度OSAHS组患者存在血管内皮功能异常,nCPAP治疗能有效修复这些损害,其机制可能与纠正间断缺氧有关.     

高血压对血管内皮功能的影响

目的:探讨高血压的血管内皮功能变化。方法:应用高分辨率超声仪检测我院门诊及住院的高血压患者的肱动脉对反应性充血(血流介导的内皮依赖性血管扩张)的舒张反应.并与健康人进行对比。结果:基础血管内径:高血压组3.89±0.47 mm.健康组3.84±0.455 mm,P>0.05;反应性充血的肱动脉内径的变化百分率:高血压组为7.4±2.83%.健康组为12.40±3.79%.有非常显著差异.P<0.001;含服硝酸甘油后肱动脉内径的变化百分率:高血压组为14.20±2.90%.健康组为14.22±0.88%(P>0.05)。结论:高血压患者血管内皮功能受损。     

彩色多普勒超声对糖尿病血管内皮功能的评价

用高分辨率彩色多普勒超声检测33例2型糖尿病(T2DM)患者肱动脉反应性充血后,以及含服硝酸甘油后的血管内径和血流量变化.结果T2DM组反应性充血时肱动脉内径变化比正常对照组明显减弱(P＜0.01),硝酸甘油介导的肱动脉内径扩张与正常对照组比较有显著性差异(P＜0.05).结论T2DM患者不仅存在血管内皮依赖性舒张功能障碍,而且还存在非血管内皮依赖性舒张功能障碍.     

高频超声评价高血压患者血管内皮功能的研究

目的:探讨高血压对血管内皮功能的影响。方法:应用高频超声检测48例原发性高血压患者和45例血压正常的健康人在静息状态、反应性充血后以及舌下含服硝酸甘油后的肱动脉内径变化。结果:原发性高血压患者反应性充血引起肱动脉内径扩张显著低于血压正常的健康人(7.62%±5.10%)vs(14.53%±3.82%),P<0.01,舌下含服硝酸甘油引起肱动脉内径扩张差异无统计学意义(18.23%±3.20%)vs(18.87%±4.35%),P>0.05。结论:原发性高血压患者存在血管内皮依赖性舒张功能受损,高频超声可以是评价血管内皮功能的无创、简单、可靠的方法。     

超声评价扩张型心肌病患者肱动脉内皮舒张功能

目的应用高频超声评价扩张型心肌病(dilated cardiomyopathy,DCM)患者肱动脉内皮功能。方法应用高频超声测量32例DCM患者和40例健康对照者的基础状态时、反应性充血后、舌下含服硝酸甘油后的肱动脉内径,计算反应性充血和含服硝酸甘油后肱动脉内径变化的百分率。结果DCM患者反应性充血所致的肱动脉内径百分变化率[(4.0±3.5)%]明显低于正常人[(13.2±3.9)%,P<0.05],DCM患者含服硝酸甘油所致的肱动脉内径变化的百分率[(27.8±9.2)%]和健康对照者[(28.5±8.9)%,P>0.05]差别无显著统计学意义。结论DCM患者肱动脉内皮舒张功能受损。     

高血压病患者血管内皮依赖性舒张功能的无创评价

目的:应用超声技术评价高血压病患者的血管内皮依赖性舒张功能.方法:用B型超声对26例高血压病患者和12例健康对照者在反应性充血和舌下含服硝酸甘油后肱动脉内径的变化情况进行了检测.结果:高血压病患者前臂加压后肱动脉内径增加的比例明显小于对照组(12.53%±4.26% vs 17.76±6.02%,P<0.01),而在舌下含服硝酸甘油后肱动脉内径的变化两组间无显著性差异(19.41%±6.73% vs 21.24%±6.96%,P>0.05).结论:高血压病患者虽然还没有明显的动脉粥样硬化的证据,但已经存在显著的血管内皮依赖性舒张功能障碍.     

彩色多普勒超声对糖尿病血管内皮功能的评价

用高分辨率彩色多普勒超声检测33例2型糖尿病（T2DM）患者肱动脉反应性充血后，以及含服硝酸甘油后的血管内径和血流量变化。结果：T2DM组反应性充血时肱动脉内径变化比正常对照组明显减弱（P〈0．01），硝酸甘油介导的肱动脉内径扩张与正常对照组比较有显著性差异（P〈0．05）。结论：T2DM患者不仅存在血管内皮依赖性舒张功能障碍，而且还存在非血管内皮依赖性舒张功能障碍。     

高血压病患者血管内皮依赖性舒张功能的无创评价

目的 :应用超声技术评价高血压病患者的血管内皮依赖性舒张功能。方法 :用B型超声对 2 6例高血压病患者和 12例健康对照者在反应性充血和舌下含服硝酸甘油后肱动脉内径的变化情况进行了检测。结果 :高血压病患者前臂加压后肱动脉内径增加的比例明显小于对照组 (12 .5 3%± 4.2 6 %vs 17.76± 6 .0 2 % ,P <0 0 1) ,而在舌下含服硝酸甘油后肱动脉内径的变化两组间无显著性差异 (19.41%± 6 .73%vs 2 1.2 4%± 6 .96 % ,P >0 0 5 )。结论 :高血压病患者虽然还没有明显的动脉粥样硬化的证据 ,但已经存在显著的血管内皮依赖性舒张功能障碍。     

X综合征患者血管内分泌功能和内皮依赖性舒张功能障碍的研究

目的　研究内皮依赖性舒张功能障碍在X综合征患者发病中的意义。方法　对 18例X综合征患者和 2 0例正常对照者 ,采用高分辨多普勒超声仪测定肱动脉基础、反应性充血和舌下含服硝酸甘油后血管舒张末期内径变化 ,并测定血浆内皮素 (ET)、一氧化氮 (NO)含量。结果　 (1)X综合征患者肱动脉血流介导的血管扩张较对照组明显减弱 ,含服硝酸甘油后血管明显扩张 ,但两组无显著差异 ;(2 )X综合征组较对照组ET水平显著升高 ,NO水平显著降低 ;(3)肱动脉血流介导的血管扩张与血浆ET水平呈显著负相关 ,与NO水平呈显著正相关。结论　X综合征患者存在血管内分泌功能紊乱、内皮依赖性舒张功能障碍 ,后者与内皮源性松弛因子减少有关。     

X综合征患者血管内分泌功能和内皮依赖性舒张功能障碍的研究

的 :研究内皮依赖性舒张功能障碍在X综合征患者发病中的意义。方法 :对 18例X综合征患者和 2 0例正常对照者 ,采用高分辨多普勒超声测定肱动脉基础、反应性充血和舌下含服硝酸甘油后血管舒张末期内径变化。并测定血浆内皮素 (ET)、一氧化氮 (NO)含量。结果 :1 X综合征患者肱动脉血流介导的血管扩张较对照组明显减弱 ,含服硝酸甘油后血管明显扩张 ,但 2组无显著差异。2 X综合征组较对照组ET水平显著升高 ,NO水平显著降低。 3 肱动脉血流介导的血管扩张与血浆ET水平呈显著负相关 ,与NO水平呈显著正相关。结论 :X综合征患者存在血管内分泌功能紊乱、内皮依赖性舒张功能障碍 ,后者与内皮源性松弛因子减少有关。     

Evaluation by high-resolution ultrasonography of endothelial function in brachial artery after Kawasaki disease and the effects of intravenous administration of vitamin C.

Previous studies in patients with a history of Kawasaki disease (KD) have focused on the endothelial function of the coronary arteries and that of the systemic arteries is not fully understood. Furthermore, the effect of vitamin C on systemic vascular endothelial function after KD has not yet been elucidated. In the present study, 39 patients (age, 7.1 +/- 2.7 years) at 1-10 years after acute KD were compared with 17 matched healthy subjects (7.0 +/- 3.1 years). High-resolution ultrasonography was used to analyze brachial artery responses to reactive hyperemia (with increased flow causing endothelium-dependent dilation) and sublingual nitroglycerin (causing endothelium-independent dilation) after KD, and to investigate whether the acute administration of vitamin C can restore systemic endothelial dysfunction. The percent change in diameter of the brachial artery induced by reactive hyperemia in the patients with a history of KD (6.2 +/- 3.9%) was significantly less than that in the control group (14.1 +/- 6.8%, p < 0.0001). No significant difference could be found in the percent change in diameter induced by sublingual nitroglycerin between the controls (33.2 +/- 13.7%) and the patients (30.6 +/- 9.2%, p = 0.49). There was no significant difference in percent change in diameter of the brachial artery induced by reactive hyperemia between the patients who received gamma globulin (6.0 +/- 4.0) and those who did not (7.9 +/- 3.3, p = 0.33). Intravenous infusion of vitamin C significantly increased the percent change in diameter of the brachial artery induced by reactive hyperemia in 19 patients with history of KD (6.6 +/- 3.5% to 13.0 +/- 5.5%, p < 0.0001). After placebo administration in 20 patients with history of KD there was no significant increase in the percent change in the diameter of the brachial artery induced by reactive hyperemia (6.5 +/- 4.5% to 7.3 +/- 4.9%, p = 0.20). The decreased percent change in the diameter of the brachial artery induced by reactive hyperemia in patients with a history of KD compared with the healthy children indicates that systemic endothelial dysfunction exists after KD. Although it is not influenced by early treatment with high-dose gamma globulin in the acute stage of KD, systemic vascular endothelial function can be restored by acute intravenous administration of vitamin C.     

Relation of vasodilator response of the brachial artery to inflammatory markers in patients with coronary artery disease

Endothelial dysfunction of the coronary artery is closely related to elevated levels of systemic inflammatory markers and cardiovascular events in patients with coronary artery disease (CAD). We hypothesized that patients with CAD may have a higher risk of endothelial dysfunction of the peripheral artery than patients without evidence of CAD, and that endothelial dysfunction of the peripheral artery also may be related to elevated levels of inflammatory markers. Using high resolution ultrasound, we assessed the brachial vasodilator response to reactive hyperemia (endothelium-dependent) and sublingual nitroglycerin (endothelium-independent). As inflammatory markers, serum C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) levels, and lipid profiles were measured in patients with CAD (n = 30, 16 male and 14 female) and normal subjects without evidence of CAD (n = 45, 23 male and 22 female). Patients with CAD (Group II) showed a significantly reduced endothelium-dependent vasodilation as compared with normal subjects (Group I) (4.4 +/- 3.6 vs 7.4 +/- 6.1%, P < 0.05). However, endothelium-independent vasodilation was not significantly different between the two groups (7.7 +/- 7.1 vs 9.7 +/- 8.0%, P > 0.05). In Group II, CRP level was inversely related to endothelium-dependent vasodilation (r = -0.398, P = 0.029). In contrast, ESR level was not significantly associated to endothelium-dependent vasodilation (r = -0.113, P = 0.552). On multivariate analysis, CRP and low density lipoprotein cholesterol levels were significant independent predictors of a blunted endothelium-dependent vasodilation in Group II. Our study showed that elevated CRP level was associated with blunted endothelium-dependent vasodilation of the brachial artery in patients with CAD. Thus, identification of elevated CRP levels combined with demonstration of endothelial dysfunction of the brachial artery may have a possible clinical application for the detection of high risk CAD patients.     

Non invasive evaluation of endothelial function in patients with Anderson-Fabry disease.

AIM: Fabry's disease is an X-linked recessive abnormality of glycosphingolipid metabolism. Increased levels of endothelial prothrombotic factors have recently been demonstrated in Fabry's disease, whereas endothelial function has not been studied using high resolution ultrasound. METHODS: We enrolled 6 patients (4 male, 2 female; mean age, 37 years) and 12 sex matched control subjects (mean age, 37 years). Patients' exclusion criteria included a prior history of cardiac disease, diabetes and treated or untreated hypertension. Patients underwent: anamnesis, physical examination, EKG, 2-dimensional echocardiography with tissue Doppler, measurement of body weight and height, blood pressure. Biochemistry variables were also considered: fasting blood sugar, total cholesterol, HDL-C, LDL-C, triglycerides, fibrinogen, C reactive protein and homocysteine. Using high resolution ultrasound, we assessed the brachial vasodilator response to reactive hyperemia (endothelium-dependent) and sublingual nitroglycerin (NTG) (endothelium-independent). Flow-mediated dilatation (FMD) was expressed as percentage change in post-stimulus diameter in comparison with the baseline. RESULTS: In baseline condition, there was no significant difference between patients and controls in the brachial artery diameter (3.5+/-0.55 vs 3.1+/-0.4). After reactive hyperemia, the FMD change was significantly higher in controls than in patients (16.5+/-6.3% vs 9.3+/-6.2%, P<0.05). After NTG, endothelium-independent vasodilation did not show a significant difference between cases and controls (15+/-7.7% vs 13.8+/-7.1%). CONCLUSIONS: Our study demonstrated the presence of endothelial dysfunction in patients with Fabry's disease in comparison to controls. We hypothesized that endothelial dysfunction may contribute to the pathogenesis of ischemic events in patients with Fabry's disease.     

高分辨率超声检测代谢综合征患者血管内皮功能

为了研究代谢综合征患者的血管内皮功能及与心血管危险因素的相关性 ,采用高分辨率超声测定 2 1例正常对照者、35例代谢综合征患者的肱动脉反应性充血及含服硝酸甘油后的血管内经和血流量的变化。结果发现 ,两组间甘油三酯、空腹血糖、餐后 2h血糖、收缩压、舒张压和体质指数差异有显著性 (P <0 .0 5或P <0 .0 1) ,而性别、年龄、总胆固醇、高密度脂蛋白胆固醇和低密度脂蛋白胆固醇差异均无显著性 (P >0 .0 5 )。两组间反应性充血后血管内径变化率、含服硝酸甘油后血管内径变化率和含服硝酸甘油后血流量变化率差异有显著性 (P <0 .0 1或P <0 .0 5 ) ,而肱动脉基础内径、肱动脉基础血流量、反应性充血后血流量、含服硝酸甘油后血流量、反应性充血后血流量变化率差异无显著性 (P >0 .0 5 )。两组反应性充血后血管内径变化率较含服硝酸甘油后血管内径变化率降低 (P <0 .0 1)。反应性充血后血管内径变化率与患者年龄 (r=- 0 .2 9,P <0 .0 5 )、甘油三酯 (r=- 0 .38,P <0 .0 5 )、收缩压 (r=- 0 .71,P <0 .0 1)、舒张压 (r=- 0 .6 1,P <0 .0 1)、空腹血糖 (r =- 0 .6 2 ,P <0 .0 1)、餐后 2h血糖 (r=- 0 .6 6 ,P <0 .0 1)和体质指数 (r=- 0 .4 7,P <0 .0 1)呈负相关。结果提示 ,代谢综合征患者存在血管内皮依     

Peripheral vascular endothelial function in essential hyperhidrosis.

BACKGROUND: Essential hyperhidrosis, a disorder of the eccrine sweat glands, is associated with sympathetic overactivity and the aim of the present study was to determine endothelium-dependent vasodilator function in patients with this condition. METHODS AND RESULTS: Using high-resolution ultrasound, the diameter of the brachial artery at rest and during reactive hyperemia (flow-mediated dilatation, %FMD endothelial-dependent stimulus to vasodilatation), as well as after sublingual administration of nitroglycerin (%NTG endothelium-independent vasodilatation) was measured in 18 subjects (mean age 27+/-5 years) with essential hyperhidrosis and 24 healthy control subjects (mean age 29+/-5 years). Baseline brachial artery diameter and FMD were comparable in both groups (BAD: 4.1+/-0.7 mm vs 4.3+/-0.5 mm (control), p = 0.8; FMD: 5.6+/-1.9% vs 6.7+/-2.2%, p=0.1). The time-averaged flow velocity during peak reactive hyperemia was similar in the 2 groups (75+/-11 cm/s vs 72+/-10 cm/s, p = 0.5), nor did NTG-induced dilatation in the patients with essential hyperhidrosis differ significantly from that in healthy control subjects (12.8+/-2.7% vs 14.0+/-3.6%, p = 0.3). CONCLUSION: These findings suggest that endothelium-dependent dilatation of large conduit arteries is preserved in essential hyperhidrosis and it seems to be a localized disorder of the eccrine sweat glands rather than a generalized disorder involving vascular endothelium.     

福辛普利对老年高血压患者内皮依赖性血管舒张功能的影响

目的探讨福辛普利对老年高血压患者内皮依赖性血管舒张功能(FMD)的影响及机制。方法应用高频彩色多普勒超声检测仪对68例老年高血压患者进行FMD的无创检查,并观察福辛普利治疗前后患者FMD的变化。结果福辛普利治疗后老年高血压患者血管内径和硝酸甘油诱发的肱动脉内径变化率与治疗前无明显差异(P>0.05),但反应性充血诱发的肱动脉内径变化率较治疗前明显增加(P<0.05)。结论老年高血压患者出现明显FMD障碍,福辛普利治疗可改善老年高血压患者血管内皮功能。     

Correlation between flow-mediated vasodilatation of the brachial artery and intima-media thickness in the carotid artery in men

Endothelial dysfunction has been reported to be the initial step in atherosclerosis. A noninvasive technique that uses ultrasound to measure the intima-media thickness of the carotid artery has been applied to evaluate localized atherosclerosis. This study was undertaken to elucidate whether endothelial dysfunction in the brachial artery is related to the intima-media thickness of the carotid artery. Thirty-four men with atherosclerosis (mean+/-SE age 61+/-2 years) and 33 age-matched men without clinical atherosclerosis were examined. The intima-media thickness and plaque formation of the common carotid artery were assessed by B-mode ultrasonography. We also noninvasively measured brachial artery diameter by the same ultrasound machine when the subjects were at rest, during reactive hyperemia, which causes endothelium-dependent vasodilatation, and after sublingual administration of nitroglycerin, which causes endothelium-independent vasodilatation. The atherosclerosis group had a significantly greater intima-media thickness of the common carotid artery than did the control group (1. 02+/-0.04 versus 0.91+/-0.03 mm, P<0.05). The flow-mediated diameter (FMD) increase (percent FMD=DeltaD/D x 100) in the atherosclerosis group was significantly smaller than that in the control group (2. 8+/-0.4% versus 5.1+/-0.6%, P<0.01). A significant negative correlation between the intima-media thickness of the carotid artery and percent FMD was found in all of the subjects. On multiple regression analysis, percent FMD showed a significant negative correlation with the intima-media thickness of the common carotid artery. These findings support the concept that endothelial dysfunction is significantly related to atherogenesis.     

Association of coronary risk factors and endothelium-dependent flow-mediated dilatation of the brachial artery.

Impaired endothelial function has been reported to be the initial step in atherosclerosis. Some coronary risk factors independently relate to impaired endothelial function. However, few studies have examined the association between coronary risk factors and endothelial function in patients who have multiple risk factors without clinical atherosclerosis. This study was undertaken to elucidate the relationship between accumulation of coronary risk factors and vascular endothelial dysfunction. We examined 101 subjects with one or more coronary risk factors 56.8 +/- 1.0 years old and 40 age-matched control subjects without coronary risk factors. We measured brachial artery diameter non-invasively using a 7.5-MHz ultrasound machine at rest, during reactive hyperemia caused by endothelium-dependent vasodilatation, and after sublingual administration of nitroglycerin, which causes endothelium-independent vasodilatation. The percentage change in flow-mediated diameter (%FMD; deltaD/D x 100), in subjects with one or more coronary risk factors was significantly lower than that in control subjects(4.8 +/- 0.3% vs. 6.7 +/- 0.5%, p < 0.01). Endothelium-independent vasodilatation by nitroglycerin did not differ between the two groups. Endothelial function was impaired according to the accumulation of coronary risk factors. On multiple regression analysis, the number of risk factors, age, and brachial artery diameter at rest showed significant correlation with %FMD. Our results suggest that an accumulation of coronary risk factors was significantly related to impairment of endothelial function.     

Endothelial function in Marfan syndrome: selective impairment of flow-mediated vasodilation

BACKGROUND: The cardiovascular complications of Marfan syndrome arise due to alterations in the structural and functional properties of fibrillin, a constituent of vascular connective tissues. Fibrillin-containing microfibrils are closely associated with arterial endothelial cells, indicating a possible functional role for fibrillin in the endothelium. Plasma concentrations of endothelial cell products are elevated in Marfan subjects, which indirectly indicates endothelial dysfunction. This study directly assessed flow- and agonist-mediated endothelium-dependent brachial artery reactivity in Marfan subjects. METHODS AND RESULTS: In 20 Marfan and 20 control subjects, brachial artery diameter, blood flow, and blood pressure were measured by ultrasonic wall tracking, Doppler ultrasound, and photoplethysmography, respectively. Measurements were taken during hand hyperemia (a stimulus for endothelium-derived nitric oxide [NO] release in the upstream brachial artery) and after sublingual administration of the endothelium-independent vasodilator nitroglycerin. In 9 Marfan and 6 control subjects, the above parameters were also assessed during intra-arterial infusions of acetylcholine and bradykinin (agonists that stimulate NO production) and NG-monomethyl-L-arginine (L-NMMA, an inhibitor of NO production). Flow-mediated responses differed markedly between Marfan and control subjects (-1.6+/-3.5% versus 6. 50+/-4.1%, respectively; P<0.0001), whereas nitroglycerin produced similar vasodilation (14.2+/-5.7% versus 15.2+/-7.8%; P=NS). Agonist-induced vasodilation to incremental intra-arterial infusions of acetylcholine and bradykinin were not significantly different between Marfan and control subjects, and intra-arterial L-NMMA produced similar reductions in brachial artery diameter in both groups. CONCLUSIONS: These data demonstrate impaired flow-mediated but preserved agonist-mediated endothelium-dependent vasodilation in Marfan subjects and suggest preservation of basal NO release. Selective loss of flow-mediated dilation suggests a role for fibrillin in endothelial cell mechanotransduction.