高血压病内皮依赖性血管舒张及分泌功能的变化

目的:探讨内皮依赖性血管舒张功能和血浆内皮素、血管性假血友病因子、纤溶酶原激活物抑制物浓度在轻、中度高血压病中的变化及其相互关系.方法:采用高分辨率超声技术,对21例轻、中度高血压病患者与21名正常对照者的内皮依赖性血管舒张功能进行检测,同时测定血浆ET-1、vWF、PAI水平.结果:高血压病组反应性充血性肱动脉舒张率较对照组明显减弱(P<0.001),而二组对硝酸甘油的反应无显著性差异(P>0.05).在高血压病组血浆vWF和ET-1水平明显高于正常对照组(P<0.05).而二组间PAI活性无显著性差异).结论:高血压病患者存在内皮依赖性血管舒张功能障碍,并有血浆ET-1、vWF水平升高,将高分辨率B超技术检测内皮依赖性血管舒张功能和血浆ET-1、vWF、PAI水平测定结合起来分析可能有利于对高血压病患者病情的判断和抗高血压药物疗效的评估.     

老年代谢综合征患者血浆同型半胱氨酸水平与血管内皮功能的研究

目的探讨老年代谢综合征(MS)患者的血浆同型半胱氨酸(Hcy)水平及血管的内皮功能。方法选择老年MS患者40例(MS组)和健康查体者36例(NC组),检测血浆Hcy水平,同时应用超声检测内皮依赖性血管舒张功能(FMD)及硝酸甘油诱导的非内皮依赖性血管舒张功能(NID)。结果MS组Hcy〔(14.7±5.2)μmol/L〕明显高于NC组〔(10.2±3.1)μmol/L〕(P<0.01),FMD〔(6.7±2.1)%〕及NID〔(9.9±3.8)%〕低于NC组〔分别为(15.4±3.2)%,(15.6±4.1)%;P<0.05,P<0.01〕。FMD与年龄、BMI、TG、SBP、DBP、FBG呈负相关。结论老年MS患者血浆Hcy水平升高,血管内皮功能失调。     

氯沙坦对高血压病患者血管内皮功能的影响及其临床意义

目的探讨氯沙坦对高血压病患者血管内皮功能的影响及其临床意义。方法采用血浆内皮素（ET）,一氧化氮（NO）,血小板α-颗粒膜蛋白（GMP140）和血管性假血友病因子（vWF）水平作为内皮功能指标,观察45例高血压病患者氯沙坦治疗4周前后血管内皮功能的改变。结果高血压组治疗前血浆ET、vWF和GMP140均显著高于正常对照组,NO/ET较正常对照显著降低（P<0.05,P<0.01）。治疗4周,高血压组的血浆ET、vWF、GMP140较前显著降低（P<0.05,P<0.01）。血浆NO及NO/ET较前显著升高,并且NO显著高于正常对照组（P<0.05,P<0.01）。ET与血总胆固醇（TC）、SBP正相关,NO和NO/ET与空腹血糖、SBP和三酰甘油显著负相关,NO/ET还与HDL正相关,vWF、GMP140与HDL负相关,GMP140与TC正相关（P<0.05,P<0.01）。结论高血压患者存在血管内皮功能减退,内皮功能与收缩压、血糖、血脂相关联。氯沙坦能够改善高血压患者的血管内皮功能。     

冠心病患者血管内皮功能障碍与动脉弹性关系的研究

目的　探讨冠心病患者血管内皮功能障碍与动脉弹性的关系。方法　采用高分辨率血管超声法检测 30例冠心病患者与 30例正常对照组肱动脉血流介导的内皮依赖性血管舒张功能(FMD);应用动脉弹性功能检测仪测定受试者的大动脉弹性指数 (C1 )和小动脉弹性指数 (C2 )。结果　冠心病组血流介导的肱动脉舒张反应明显低于对照组[ (5 17±2 13)% 与 (11 10±4 36)%,P<0 05];冠心病组与正常对照组的C1 差异无统计学意义 [ ( 11 59±4 56 )ml/mmHg( 1mmHg=0 133kPa) ×10与 (12 11±3 82)ml/mmHg×10, P>0 05],但冠心病组的C2 明显低于正常对照组[ (4 20±1 80)ml/mmHg×100与 (6 26±2 36)ml/mmHg×100, P<0 05],冠心病组血流介导的肱动脉舒张反应与C2 呈正相关(r=0 53, P<0 05)。结论　冠心病患者肱动脉内皮依赖血管舒张功能受损和C2 降低,且两者之间呈正相关,提示C2 可作为一种评价血管内皮功能的新指标。     

充血性心力衰竭患者口服ACEIs后血浆ox-LDL、vWF及TAC改变的临床意义

目的本研究观察了67例充血性心力衰竭（CHF）患者口服培哚普利和依那普利后血浆氧化型低密度脂蛋白（ox-LDL）、血管性假血友病因子（vWF）及总抗氧化能力（TAC）的改变,探讨血管紧张素转换酶抑制剂（ACEIs）对体内氧化状态和血管内皮功能的影响。方法67例CHF患者随机给予依那普利或培哚普利治疗8周后,观察血浆ox-LDL、vWF及TAC水平的改变。35例健康志愿者作为正常对照组。血浆vWF和ox-LDL采用酶标法测定,血浆TAC水平采用分光光度计测定。结果两组CHF患者基础血浆ox-LDL、vWF水平高于健康对照组（P<0.01）,血浆TAC水平低于正常对照组（P<0.01）;服药4周后,依那普利组和培哚普利组血浆ox-LDL、vWF水平下降（P<0.05）,8周后进一步下降（P<0.01）;而血浆TAC水平在4周时升高（P<0.05）,8周时进一步升高（P<0.01）。结论ACEIs如依那普利和培哚普利能提高CHF患者的抗氧化能力,改善血管内皮功能以及降低血栓形成倾向,从而对阻断CHF的恶性循环起到有益作用。     

普伐他汀对不稳定性心绞痛患者血管内皮功能的影响

目的　探讨普伐他汀对不稳定性心绞痛 (UA)患者血管内皮依赖性舒张功能和纤溶系统的影响。方法　采用高分辨超声技术 ,将 42例 AU患者按随机编码分为普伐他汀组和对照组 ,观察降脂治疗前后血管内皮依赖性舒张功能和血浆纤溶酶原激活物 (t PA)及其抑制物 (PAI)活性。结果　普伐他汀组与对照组和治疗前比较 ,血流介导的肱动脉舒张百分率显著增加 ,(9.5± 3.2 ) %和 (5.0± 2 .2 ) %、(4.2± 2 .0 ) % (均 P<0 .0 1 )。血浆 t PA活性增强 ,(0 .48± 0 .1 7) IU/ml和 (0 .352± 2 .0 ) IU/ml、(0 .2 75± 0 .1 5) IU/ml(P<0 .0 1 ) ;血浆 PAI活性减弱 (0 .350± 0 .1 0 5) AU/ml和 (0 .450± 0 .1 2 ) AU/ml、(0 .52 5± 0 .2 5) AU/ml(均 P<0 .0 5)。线性相关分析显示 :血流介导的肱动脉舒张百分率及血浆纤溶活性改变与血脂的降低无关。结论　普伐他汀能改善 UA时受损的血管内皮依赖性舒张功能和血浆纤溶活性。     

X综合征患者内皮素-1及血管内皮依赖性舒张功能的变化

目的 :观察 X综合征患者内皮素 - 1( ET- 1)及血管内皮依赖性舒张功能变化。　　方法 :采用高分辨超声技术检测 15例 X综合征患者 ( X综合征组 )血管内皮依赖性舒张功能 ,并测定其血中 ET- 1含量 ,与 2 0例正常人 (正常对照组 )进行对照。　　结果 :1X综合征组患者反应性充血引起的肱动脉内径变化较正常对照组明显减弱 [( 4 .2± 2 .1) %比 ( 13 .6±3 .2 ) % ,P<0 .0 0 1],而两组患者对硝酸甘油的反应无显著性差异 [( 2 1.6± 7.8) %比 ( 2 2 .8± 4 .7) % ,P>0 .0 5 ]。 2 X综合征组患者在胸痛前、胸痛发作时及胸痛后的 ET- 1含量均较正常对照组明显升高 ( 6.74± 2 .4 1ng/ L ,10 .0 7± 1.93 ng/L及 7.4 2± 2 .2 4 ng/ L比 4 .13± 1.3 6ng/ L ,P<0 .0 1)。胸痛发作时 ET- 1含量较胸痛前及胸痛后亦有明显差异 ( P<0 .0 1)。 3肱动脉内皮依赖性舒张功能变化与 ET- 1含量呈显著的负相关 ( r=- 0 .73 2 8,P<0 .0 0 1)。　　结论 :X综合征患者存在明显的血管内皮依赖性舒张功能障碍 ,心绞痛发作和 ET- 1水平增高有关。提示内皮功能异常在 X综合征患者的发病过程中起重要作用。     

阻塞性睡眠呼吸暂停低通气综合征患者的血管内皮舒张功能

目的评价阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者的血管内皮功能。方法OSAHS患者30例(轻度组8例,中重度组22例)及对照组10例,分别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)以及含服硝酸甘油后(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。结果对照组、轻度和中重度OSAHS组患者反应性充血时肱动脉内径扩张率分别为(15.2±2.6)%、(14.3±3.2)%和(9.8±4.9)%,中重度OSAHS组患者血管内皮介导的舒张反应较对照组和轻度OSAHS组明显降低;含服硝酸甘油后肱动脉内径扩张率分别为(16.5±5.0)%、(15.7±4.1)%和(14.1±6.2)%,3组间无明显差别。结论中重度OSAHS患者存在血管内皮功能障碍,OSAHS本身可能是导致血管内皮损伤的重要因素。     

心力衰竭治疗前后血浆白细胞介素-18的变化及临床研究

目的 探讨不同级别心功能衰竭(CHF)患者治疗前、后血浆白细胞介素-18(IL-18)水平的临床意义.方法 采用酶联免疫法(ELAsA)检测116例CHF患者血浆IL-18水平,并以31例健康者作对照,分析CHF患者治疗前、后心功能分级与血浆IL-18水平的变化.结果 CHF患者血浆IL-18水平显著高于对照组[(570.99±63.18)pg/ml和(201.82±46.09)pg/ml,(595.24±74.33)pg/ml和(201.82±46.09)pg/ml,(657.07±73.86)pg/ml和(201.82±46.09)pg/ml,F=6.68,P＜0.01].经过治疗心功能改善后血浆IL-18水平显著下降(t=4.56,5.99,3.22,3.78,P＜0.01).结论 IL-18可能参与CHF的发生及发展过程,监测血浆水平对判断心衰、指导治疗、评价疗效有一定参考价值.     

急性冠状动脉综合征患者降胆固醇治疗对内皮依赖性血管舒张功能、血小板及纤溶活性的影响

目的探讨急性冠状动脉综合征降低胆固醇水平后对内皮依赖性血管舒张功能、血小板表面活性颗粒膜蛋白(CD63)、溶酶体膜蛋白(CD62P)及血浆纤溶酶原激活物抑制物-1(PAI-1)的影响.方法70例急性冠状动脉综合征患者随机分成普伐他汀治疗组(普伐他汀组)38例及常规治疗组(常规组)32例,比较观察治疗6周前后应用超声检测肱动脉流量介导性扩张(FMD)的血管内皮舒张功能,血小板CD63、CD62P含量及血浆PAI-1、内皮素-1(ET1)水平的变化.结果(1)治疗前两组比较,内皮依赖性血管舒张功能差异无显著性[(4.91±0.81)%与(4.93±0.86)%,P＞0.05];治疗6周后,常规组内皮依赖性血管舒张功能较治疗前差异无显著性[(5.25±0.77)%与(4.93±0.86)%,P＞0.05],而普伐他汀组治疗后差异有十分显著性[(6.92±0.94)%与(4.91±0.81)%,P＜0.01].(2)普伐他汀组治疗6周后血小板CD63、CD62P及血浆PAI-1、ET-1各项指标较治疗前[(15.48±3.94)%、(14.97±3.24)%、(11.73±3.18)Au/ml、(5.97±2.84)ng/L]均有不同程度降低[(10.12±2.92)%、(10.46±3.45)%、(8.12±2.72)Au/ml、(3.28±1.85)ng/L,P＜0.01].结论急性冠状动脉综合征患者在降胆固醇治疗6周后可改善内皮依赖性血管舒张功能,同时抑制血小板活性,改善纤溶活性.     

Increased plasma levels of endothelin-1 and urotensin-II in patients with coronary heart disease

Research has identified the vasoconstrictors endothelin-1 (ET-1) and urotensin-II (U-II) as having a role in the development of atherosclerotic cardiovascular disease. We aimed to observe alterations in plasma levels of both ET-1 and U-II in patients with coronary heart disease (CHD) undergoing percutaneous transluminal coronary angioplasty (PTCA) and stent therapy from November 2006 through May 2007. We examined plasma levels of ET-1 and U-II in 40 patients with CHD and 40 age-matched healthy subjects by radioimmunoassay (RIA). Chi-square test, Student’s t-test, and one-way analysis of variance were used for statistical analyses. Correlations between variables were tested by simple linear regression analysis. Coronary heart disease patients had significantly higher ET-1 and UII levels than healthy controls (20.05 ± 4.65 vs 8.16 ± 3.38 and 71.90 ± 11.61 vs 20.89 ± 7.00 pg/ml, respectively, all P < 0.01). Importantly, plasma levels of U-II and ET-1 were correlated in patients with CHD (r = 0.64, P = 0.01). On day 1 after PTCA and stent therapy, plasma levels of ET-1 and U-II were significantly higher, by 99% and 25%, respectively, than those before therapy (all P < 0.01). On day 3 after therapy, ET-1 levels were higher by 25% (P < 0.01) than before therapy, and U-II levels decreased rapidly and were close to baseline levels (P > 0.05). On day 7 after therapy, CHD patients had significantly lower ET-1 and U-II levels than before therapy (all P < 0.01). Since ET-1 and U-II levels may be increased in plasma of patients with CHD, their activation might have clinical significance in terms of early intervention in patients with CHD, especially after PTCA and stent therapy.     

Endothelial Markers in Schistosomiasis Patients With or Without Portal Hypertension

Purpose To evaluate the serum levels of von Willebrand factor (vWF), vascular endothelial growth factor (VEGF), endothelin-1 (ET-1), and endothelin-3 (ET-3) in patients with the isolated, inactive form of Schistosomiasis mansoni. Patients were classified into two groups: 10 patients without (SM group) and 18 with (PH group) portal hypertension. Results Serum albumin, VEGF, and vWF levels did not differ between the two groups (P > 0.05). The prothrombin time (INR), number of platelets, spleen size, splenic vein diameter, and endothelin levels differentiated the PH group, which showed decreased ET-1 (SM = 22.4 ± 2.4 pg/ml and PH = 16.4 ± 1.5 pg/ml; P = 0.034) and increased ET-3 (SM = 2.1 ± 0.1 ng/ml and PH = 3.2 ± 0.1 ng/ml; P = 0.000) levels. Conclusions In patients with schistosomiasis and portal hypertension (presinusoidal type), the levels of VEGF and ET-1 differ from those reported in patients with cirrhosis.     

Endothelial Dysfunction in Patients with Noncomplicated and Complicated Hypertension

Endothelial dysfunction plays an important role in the pathogenesis of hypertension. Other risk factors of atherosclerosis also affect its development. The aim of the study was to assess nitric oxide metabolites concentration (nitrites and nitrates No_x) and endothelin (ET-1) in plasma and cyclic 3,5-guanosine monophosphate (cGMP) in 24 h-urine collection in patients with noncomplicated hypertension without risk factors of atherosclerosis and in hypertensive patients with coronary artery disease (CAD). Sixty-eight subjects were included in the study (44 men, 24 women), aged 47 ± 76 years, allotted into four groups: I – controls (18 clinically healthy subjects); II – 12 subjects with hypertension without risk factors of atherosclerosis; III – 16 subjects with hypertension and risk factors of atherosclerosis; and IV – 22 subjects with hypertension and CAD. Plasma NO_x concentration was determined using the Greiss method, plasma ET-1 by ELISA, and urine cGMP using the immunoenzymatic method. Plasma NO_x concentration was 14.00 ± 6.88 μmol/L in group I, in group II – 18.62 ± 5.84 μmol, in group III – 9.96 ± 4.72 μmol/L, and in group IV – 8.78 ± 3.72 μmol/L. Statistically significant differences were between groups I and III (p < 0.05) and I and IV (p < 0.04) and groups II and III (p < 0.01) and II and IV (p < 0.01). The concentration of cGMP in 24 h urine collection was in group I – 40 ± 24 pmol/L; in group II – 54 ± 41 pmol/L; in group III – 38 ± 32 pmol/L; and in group IV – 42 ± 36 pmol/L. There were no significant differences between the groups. Plasma ET-1 concentration was 3.86 ± 0.52 pg/mL in group I, in group II – 4.05 ± 0.71 pg/mL, in group III – 4.22 ± 0.79 pg/mL and in group IV – 4.38 ± 0.75 pg/mL. Statistically significant differences were between group I and III (p < 0.05), I and IV (p < 0.03), and between group II and IV (p < 0.04). Endothelial dysfunction was not found in hypertensive patients without a family history of cardiovascular diseases and without other risk factors of atherosclerosis. Deterioration of endothelial function was observed in patients with hypertension with risk factors of atherosclerosis. It was most pronounced in those with CAD.     

Interdependence of Cardiac and Endothelial Function in Patients with Symptomatic Chronic Heart Failure of Nonischemic Etiology

Objective: Endothelial dysfunction has emerged as a therapeutic target in patients with chronic congestive heart failure (CHF). Endothelial dysfunction may impair left ventricular (LV) systolic function by increasing systemic vascular resistance. Conversely, LV impairment may negatively impact endothelial function by reducing shear stress and vascular nitric oxide (NO) bioavailability. This study was undertaken to determine the association between LV and endothelial function in patients with CHF. Methods: Echocardiographic and vascular ultrasound studies were performed to measure left ventricular ejection fraction (LVEF) and brachial artery flow-mediated vasodilatation (FMD) in 30 subjects with stable New York Heart Association class II–III CHF. All patients received optimal medical therapy. Results: LVEF averaged 25 ± 9% and brachial artery FMD 1.3 ± 2.4%. LVEF strongly correlated with FMD among all patients (r = 0.64, P< 0.001) and among those patients with nonischemic (n = 19, r = 0.66, P = 0.002), but not in patients with ischemic etiology (n = 11, r = 0.27, P = 0.42). Conclusions: LVEF and endothelium-dependent NO vasodilatation are strongly correlated in stable ambulatory patients with systolic CHF of nonischemic etiology. Our study underscores the mutual interaction between central cardiac and peripheral vascular function, thus strengthening a mechanistic rationale for the systemic beneficial effects of interventions targeting either the heart or the vascular endothelium in CHF.     

Association between Endothelial Function and Chronotropic Incompetence in Subjects with Chronic Heart Failure Receiving Optimal Medical Therapy

Objective: Impairment of flow‐mediated, endothelium‐dependent vasodilatation (FMD) of the brachial artery identifies peripheral endothelial dysfunction in subjects with chronic congestive heart failure (CHF) and is associated with increased morbidity and mortality. To further elucidate the interaction of peripheral and central mechanisms in the syndrome of CHF, we examined the association between endothelial function and chronotropic incompetence, an emerging prognostic marker in CHF. Methods: Thirty subjects with stable New York Heart Association (NYHA) functional class II–III CHF were studied. A vascular ultrasound study was performed to measure brachial artery FMD. The percentage of age‐adjusted maximal predicted heart rate (MPHR) reached during cardiopulmonary exercise tolerance testing (CPETT) was used to assess the degree of chronotropic competence. All patients received ACE inhibitors and β‐adrenoceptor blockers. Results: Brachial artery FMD averaged 1.3 ± 2.4% and age‐adjusted % MPHR 74.1 ± 11.7%. FMD correlated with % MPHR among all patients (r = 0.60, P = 0.01). FMD and resting heart rate (RHR) did not significantly correlate (r = 0.13, P = 0.55). Conclusions: FMD, a measure of peripheral endothelial dysfunction, and % MPHR, a central determinant of cardiac output, are moderately correlated in heart failure patients receiving optimal medical therapy. Whether a cause‐effect relationship underlies this association remains to be investigated. (Echocardiography 2010;27:294‐299)     

Angiopathy affects circulating endothelin-1 levels in type 2 diabetic patients

To evaluate the role of endothelin-1 (ET-1), a vasoconstrictor and mitogenic peptide synthesized by endothelial cells, on the endothelial dysfunction in non-insulin-dependent diabetic (type 2) patients, we have measured the circulating ET-1 levels in 25 patients with and without clinically evident vascular complications and in a control group. Circulating ET-1 levels were significantly higher in diabetic patients with angiopathy than in diabetics without angiopathy and in controls (7.02±2.9 pg/ml vs 4.4±1.1 pg/ml and 3.08±0.7 pg/ml, respectively;P<0.001). No difference was demonstrated between diabetic patients without angiopathy and controls. These findings suggest that ET-1 may be a marker for arterial vascular disease only in patients with overt angiopathy. It is unclear whether it participates in the endothelial injury process or it is merely released from damaged endothelial cells.     

EFFECT OF NICARDIPINE VERSUS ENALAPRIL ON PLASMA ENDOTHELIN-1 IN HYPERTENSIVE PATIENTS WITH TYPE 2 DIABETES MELLITUS

We compared the effects of dihydropyridine type Ca channel blocker slow-release nicardipine and angiotensin converting enzyme inhibitor enalapril on plasma endothelin-1 (ET-1) levels in hypertensive type 2 diabetic patients (n = 20). Nicardipine or enalapril was administered for 6 months by a crossover design. Nicardipine and enalapril comparably lowered blood pressure. Enalapril significantly reduced urinary albumin excretion in microalbuminuric patients, whereas nicardipine did not. Urinary β2-microglobulin excretion was significantly increased during nicardipine treatment. However, both drugs significantly reduced plasma ET-1 as compared with pretreatment levels, close to that in healthy control (2.9 ± 0.3 pg/ml in control, 4.8 ± 0.3 pg/ml before treatment, 3.2 ± 0.3 pg/ml during nicardipine vs before treatment p<0.05, 2.9 ± 0.4 pg/ml during enalapril vs before treatment p<0.01). The decrease in plasma ET-1 was significantly correlated with the increase in natriuresis in normoalbuminuric patients treated with enalapril (r=?0.82, p<0.01) but not in those treated with nicardipine. Although nicardipine and enalapril had different renal effects, both drugs equally suppressed plasma ET-1 levels in hypertensive patients with type 2 diabetes.     

B型利钠肽测定对充血性心力衰竭患者预后评估的研究

目的探讨B型利钠肽(BNP)对充血性心力衰竭(CHF)患者预后评估的价值。方法对343例因CHF住院的患者,入院时测定BNP,同时测定左心室射血分数(LVEF)、左心室舒张末内径(LVDD),胸片测定心胸比率(CTR)。出院前复查一次,随访观察患者3个月内的病死率、再住院率,作为终末事件。结果①心功能Ⅰ、Ⅱ、Ⅲ、Ⅳ级患者的BNP水平分别为(157±15)pg/ml、(341±22)pg/ml、(597±33)pg/ml、(1245±38)pg/ml。心功能越差,BNP越高,不同的NYHA心功能分级,BNP差异有显著性(P<0.001)。②BNP水平与LVEF呈明显负相关(r=-0.8,P<0.05)。③343例患者,住院期间死亡5例,3月内再次入院22例。事件组27例,其BNP水平为(1683±124)pg/ml,非事件组316例,其BNP水平为(468±48)pg/ml。两组差异有显著性(P<0.001)。4.将出院前BNP>1500pg/ml作为评估终末事件的界值,其预测预后的敏感性为96.3%,特异性为92.7%。5.对CHF患者的性别、年龄、LVEF、LVDD、BNP、病因等进行多元逐步回归分析,BNP与预后关系最密切。结论本文提示BNP较LVEF评价CHF更确切可靠,动态观察BNP变化水平是CHF患者有效的预后判断指标。     

17-β雌二醇对培养人脐静脉内皮细胞缺氧损伤的保护作用

目的探讨缺氧对培养人脐静脉内皮细胞(HUVECs)的损伤及17-β雌二醇(E2)对其保护作用。方法胰蛋白酶灌流消化法培养原代人脐静脉内皮细胞,建立细胞缺氧模型。随机分为五组:对照组、缺氧12h组、缺氧24h组、E2+缺氧12h组、E2+缺氧24h组。对照组为常氧下培养的HUVECs,缺氧组按缺氧模型予缺氧下培养HU-VECs,E2+缺氧组予预先加入17-βE2后再缺氧下培养HUVECs。收集各组细胞培养液,Greiss反应测定一氧化氮(NO),放射免疫法测内皮素-1(ET-1);收集各组HUVECs,进行细胞计数,细胞骨架染色观察细胞形态。结果缺氧12h,内皮细胞数由对照组(4.33±0.24)×106/ml减少至(3.23±0.21)×106/ml(P<0.01),形态无明显变化;其分泌NO由对照组(19.28±2.08)nmol/106cell下降至(12.77±1.90)nmol/106cell(P<0.01),ET-1由对照组(95.7±11.32)pg/ml上升至(138.3±10.37)pg/ml(P<0.01)。缺氧24h,内皮细胞数由对照组(4.33±0.24)×106/ml减少至(2.73±0.19)×106/ml(P<0.01),形态变长体积变小;其分泌NO由对照组(19.28±2.08)nmol/106cell下降至(10.76±1.57)nmol/106cell(P<0.01);ET-1由对照组(95.7±11.32)pg/ml上升至(150.1±15.41)pg/ml(P<0.01)。经预先17-βE2处理后能有效抑制上述改变(P<0.01)。结论缺氧可使内皮细胞结构和功能均受损,17-βE2对这种缺氧损伤有保护作用。     

卡维地洛对慢性心衰患者糖、脂代谢的影响

目的观察卡维地洛对慢性心衰患者的疗效及其对血糖,血脂代谢的影响。方法入选CHF患者59例,随机分为对照组:应用常规抗CHF治疗组(30例)和卡维地洛组(29例),后者在常规抗CHF治疗基础上加用卡维地洛,疗程为24周,治疗前后均测定左室舒张末期内径(LVDd)和收缩末期内径(LVDs)、左室射血分数(LVEF)、空腹血糖(FBS)、糖化血红蛋白(HbAlc)、血脂。结果卡维地洛组改善LVDd、LVDs和LVEF均优于常规抗CHF治疗组(P<0.01),治疗后卡维地络组TC、LDL-C较对照组降低(P<0.05)。结论卡维地洛可有效改善CHF患者的心功能,对糖、脂代谢有一定的益处。