缺氧对肺动脉内皮细胞和平滑肌细胞分泌血管活性肽的影响

用放射免疫测定和免疫组化法缺氧对培养的小牛肺动脉内皮细胞（ＰＡＥＣ）和肺动脉平滑肌细胞（ＰＡＳＭ）自分泌心钠素（ＡＮＰ）、血管紧张素Ⅱ（ＡＴⅡ）和内源性洋地黄因子（ＥＤＬＦ）的影响。无氧培养２４ｈ末，ＰＡＥＣ分泌ＡＮＰ减少４３．５％（Ｐ〈０．００１），ＡＴⅡ和ＥＤＬＦ呈明显负相关（ｒ为－０．８８和－０．７８６，Ｐ〈０．０１），细胞内ＡＮＰ阳性颗粒也显著减少（Ｐ〈０．００１）；ＰＡＳＭ分泌ＡＮＰ无显     

肺动脉血管紧张素转换酶在缺氧性肺动脉高压演进过程中的作用

为了探讨肺动脉局部肾素血管紧张素系统对缺血性肺动脉高压（PAH）的影响，作者采用常压缺氧PAHWis－tar大鼠动物模型随机分组，观察缺氧后肺动脉收缩压（PAPs）、肺动脉血管紧张素转换酶（ACE）活性、胶原蛋白含量（HP）及血管平滑肌细胞（SMC）超微结构的变化，以及ACE抑制剂──西拉普利对以上变化的影响．结果显示：缺氧期间PAPs、ACE活性、HP显著增高，SMC转为分泌型；缺氧组血清ACE活性（SACE）显著下降，PAPS、肺动脉ACE活性（pACE）、羟脯氨酸含量（HP）随缺氧时间延长进行性增高，并高于对照组；自然恢复6周…     

特技飞行对血清胰岛素、皮质醇、血管紧张素Ⅱ和胃泌素的影响

为观察特技飞行对胰岛素、皮质醇、血管紧张素Ⅱ和胃泌素等激素的影响。２０名健康男性飞行员（年龄２４～３０岁），复杂特技飞行时最大加速度为＋６．０Ｇｚ，分别在飞行前２ｈ，飞行后即刻、６ｈ及飞行后２４ｈ采血。用放射免疫法测定上述激素。结果发现，飞行后即刻血清胰岛素含量（２６．４±３．６８μＩＵ／ｍｌ）较飞行前（１３．１±０．４８μＩＵ／ｍｌ）有明显升高（Ｐ＜０．０１），飞行后２４ｈ胰岛素含量（１７．２±１．３７μＩＵ／ｍｌ）明显下降，与飞行后即刻比较有显著性差异（Ｐ＜０．０５），但与飞行前比较，无显著性差异（Ｐ＞０．０５）。飞行后即刻６ｈ血清胃泌素明显升高（９６．４±２２．０，１１０．７±２８。７ｐｇ／ｍｌ）与飞行前（３５．３±１５，０ｐｇ／ｍｌ比较，有显著差异（Ｐ＜０．０５）。飞行后２４ｈ血清胃泌素明显下降，与飞行后即刻比较有显著差异（Ｐ＜０．０５）。飞行前后血清皮质醇和血管紧张素Ⅱ均无显著性变化（Ｐ＞０．０５）。飞行后即刻胰岛素及胃泌素含量均明显高于飞行后２４ｈ，二者同为上午１０时抽取的标本，说明其升高不是正常日节律所致，与饮食亦无明显关系。有研究发现，特技飞行后即刻血液中胃动素含量明显升高，胃动素能促进胰岛     

右旋糖酐加脑组织注射液治疗高原肺心病高粘状态疗效观察

对高海拔地区１５例慢性肺心病凝患者用低分子右旋糖酐５００ｍｌ加脑组织注射液２０ｍｌ，静滴，１次／日，１５天为一疗程进行治疗前后对比观察结果显示：血液流变学指治疗后较治疗前差异极为显著（Ｐ〈０．０５－０．００１）；ＰａＯ２、ＳａｔＯ２治疗后较治疗前上升明显（Ｐ〈０．０５）ＰａＣＯ２治疗后明显下降（Ｐ〈０．０１）；未发现不良反应。为此，本疗法对降低血液粘度及血管阻力，改善微循环及组织低氧状态，增加脑组     

高原慢性肺源性心脏病血清酶活性与病情及预后的关系

目的：探讨高原肺心病血清酶活性变化与病情、血气及预后的关系。方法：５６例高原（２２６０～３２００ｍ）慢性肺心病患者在急性发作期和缓解期测定了血清肌酸激酶（ＣＫ）、谷草转氨酶（ＡＳＴ）、γ－谷氨酰转肽酶（γ－ＧＴ）和乳酸脱氢酶（ＬＤＨ）活性。结果：结发期４种血清酶活性均显著高于缓解期，缓解期显著高于健康对照组（Ｐ均〈０．０１），呼吸衰竭组４种血清酶活性显著高于无呼衰组（Ｐ〈０．０１或〈０．０５）。呼     

进驻海拔5000m以上地区一年青年心脏体积X线观察

本文对进驻海拔５０００ｍ以上地区一年的５８名青年在现场拍摄正、侧位Ｘ线胸片并与平原时相比较，结果：心脏长径及心胸比率显著较小（Ｐ〈０．００１）；心脏面积缩小，但相关不显著（Ｐ〉０．０５）；心脏宽径，心脏深径、心脏体积及心脏体积指数显著增加（Ｐ〈０．００１或Ｐ〈０．０１）；右心房宽径、右心房高径、左室壁厚度、肺面积、升主动脉模径、主动脉结构横径、肺动脉干横径、肺动脉段突度，右肺下动脉横径及右肺下动脉     

海拔5200m重体力劳动45天心肺X线改变及对劳动能力的影响

作者对海拔５２００ｍ从事重体力劳动４５天的４８名青年在劳动前后现场摄取Ｘ线胸片。结果：心脏横径、心脏长径、心脏面积、心胸比率较初入高原时显著缩小（Ｐ〈０．０１）；肺动脉干横径、肺动脉段突度、右肺下动脉横径、右肺下动脉与气管横径比值显著增加（Ｐ〈０．０１）；升主动脉和主动脉横径、胸宽和肺面积增加或显著增加（Ｐ〈０．０５或Ｐ〈０．０１）。其中２例诊断为高原性心脏病，３例诊断为高原性肺水肿。在海拔５２０     

慢性缺氧大鼠肺动脉胶原堆积与肺动脉ACE活性的相关分析

慢性缺氧大鼠肺动脉胶原堆积与肺动脉ＡＣＥ活性的相关分析５１００１０广州广州军区广州总医院蔡闯邹霞英辛达临赖日权关键词缺氧症；胶原；血管紧张素转换酶；肺动脉高压中国图书资料分类号Ｒ３６４．４研究表明，心血管肾素血管紧张素系统（ＲＡＳ）与高血压、主动脉血...     

飞行条件对飞行员血浆神经肽的影响

对４８例患心血管疾病的飞行员进行了血浆神经肽中心房利钠多肽（ＡＮＦ）、精氨酸加压素（ＡＶＰ）、神经降压素（ＮＴ）、血管活性肠肽（ＶＩＰ）４种心血管调节肽飞行前后动态观察，并与３７例健康飞行员进行比较。结果，两组飞行员飞行后ＡＮＦ、ＡＶＰ均较飞行前显著升高（Ｐ＜０．０５）；ＶＩＰ、ＮＴ飞行前后均无显著性差异（ｐ＞０．０５）。飞行前后实验组ＡＶＰ均显著地高于对照组（Ｐ＜０．０５）；ＶＩＰ显著低于对照组（Ｐ＜０．０５）；两组ＡＮＦ、ＮＴ无显著差异（Ｐ＞０．０５）。结果提示，对飞行员早期心血管疾病患者，只要注意治疗，稳定病情，飞行负荷对其不会有大的生理影响和改变。     

慢性缺氧性肺动脉高压大鼠内皮素肾素血管紧张素变化

缺氧肺动脉高压的原因仍未明了,内皮素和血管紧张素Ⅱ不仅能使血管强烈收缩,而且还能促进血管平滑肌、心肌等细胞的生长,参与血管和心肌的重构,在肺动脉高压的发生发展中起着重要的作用,此研究从组织局部的角度,研究了局部肾素血管紧张素系统（ＲＡＳ）和内皮素对缺氧性肺动脉高压（ＰＡＨ）的影响。采用常压缺氧ＰＡＨ动物模型、观察血液、右心室、肺组织肾素活性（ＲＡ）、血管紧张素Ⅱ（ＡｎｇⅡ）、血管紧张素转换酶（ＡＣＥ）及内皮素（ＥＴ）含量变化和西拉普利（ｃｉｌａｚａｐｒｉｌ）的治疗作用。结果发现缺氧时血ＲＡ５对照…     

Renin angiotensin aldosterone system and ACE I/D gene polymorphism in high-altitude pulmonary edema

INTRODUCTION: People who visit high altitude are exposed to a stressful environment, and many of them suffer from altitude-induced conditions, including high altitude pulmonary edema (HAPE). We investigated the renin angiotensin aldosterone system (RAAS) and the possible association of angiotensin converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism in the development of HAPE in Indian men. METHODS: Subjects were all low-altitude natives: 19 men who developed HAPE within 1-3 d of arrival at 3000 to 3800 m (patients); and 20 age-matched men who did not develop HAPE during a period of a month or more at > or = 3500 m (controls). We recorded the arterial oxygen saturation (Sao2), heart rate (HR), and blood pressure (BP) of both groups and measured their levels of plasma renin activity (PRA), ACE, aldosterone, and serum electrolytes. Polymerase chain reaction was used to investigate a 287 base pair alu repeat sequence I/D polymorphism in the ACE gene. RESULTS: Compared with controls, patients showed a significantly lower Sao2 and a higher HR. They also had significantly higher plasma PRA, aldosterone, ACE, and serum sodium (Na+) and potassium (K+). No significant difference was observed in ACE I/D allele frequencies. DISCUSSION: The results suggested that RAAS is involved in the development of HAPE in low-altitude natives, but there is no association of ACE I/D gene polymorphism with HAPE.     

氧化应激在低压缺氧性肺动脉高压形成中的作用

目的观察低氧对血清中活性氧(ROS)水平的影响,探讨氧化应激在低压缺氧性肺动脉高压形成中的作用。方法将24只Wistar大鼠随机分为平原对照组(C组),缺氧组(H组),N-乙酰半胱氨酸组(N组),缺氧+N-乙酰半胱氨酸组(H+N组)。建立低压缺氧模型21 d后,测定其右心室收缩压(RVSP)和平均肺动脉压(mPAP);HE染色观察各组大鼠的肺动脉壁厚度;比色法测定血清中ROS的含量。结果与C组相比,H组RVSP、mPAP明显升高(均P<0.05),HE染色示H组肺动脉壁增厚,且血清中ROS水平明显升高(P<0.05);给予ROS清除剂NAC后,RVSP及mPAP降低,肺血管重塑减弱。结论低氧时氧化应激参与了低压缺氧性肺动脉高压的形成。     

Structure-function analysis of angiotensin-converting enzyme inhibitors as modifiers of radiation-induced pulmonary endothelial dysfunction in rats

We have previously demonstrated that thiol-containing collagen antagonists (penicillamine) and angiotensin-converting enzyme (ACE) inhibitors (Captopril and CL242817) ameliorate endothelial dysfunction in irradiated rat lung. The purpose of the present study was to determine whether the non-thiol ACE inhibitor CGS13945 also modifies radiation-induced pulmonary endothelial dysfunction in rats sacrificed 2 months after a single dose (0-30 Gy) of 60 Co gamma rays to the right hemithorax. The CGS13945 was administered in the feed continuously after irradiation at a regimen of 30 mg (kg body weight)-1 day-1. Four markers of lung endothelial function were monitored: ACE activity, plasminogen activator (PLA) activity, and prostacyclin (PGI2) and thromboxane (TXA2) production. Right lung ACE and PLA activities decreased with increasing radiation dose, and CGS13945 significantly ameliorated both responses. Dose-reduction factors (DRF) for the inhibitor were 1.80 for ACE activity and 1.41 for PLA activity (p less than 0.05). In contrast, lung PGI2 and TXA2 production increased with increasing radiation dose, and CGS13945 did not influence either response significantly. Thus the ACE inhibitor CGS13945 modifies radiation-induced pulmonary endothelial dysfunction in rats, indicating that the presence of a thiol group is not essential for therapeutic efficacy in this class of compounds. On the other hand, CGS13945 exhibits a differential sparing of radiation-induced pulmonary endothelial dysfunction, as does penicillamine. A structure-function analysis of the present and previous data indicates that all of the ACE inhibitors tested (Captopril, CL242817 and CGS13945) spare the radiation-induced suppression in lung ACE and PLA activity; all of the thiol compounds tested (penicillamine, Captopril and CL242817) spare the radiation-induced elevation in lung PGI2 and TXA2 production; and the thiol ACE inhibitors (Captopril and CL242817) spare all four endothelial responses. These data confirm a novel and potentially important application for ACE inhibitors as modifiers of radiation-induced lung injury, and suggest that there are at least two components to their mechanism of therapeutic action in this model.     

血管紧张素转换酶基因多态性及血清水平与原发性高血压并发脑梗死的关系

目的　研究血管紧张素转换酶 (ACE)基因多态性及血清ACE水平与原发性高血压并发脑梗死的关系。方法　采用聚合酶链反应对 153例观察对象 (正常对照 51例,高血压 47例,原发性高血压并发脑梗死 55例 )的ACE基因进行分型,并测定血清ACE活性。结果　153例受检者中ACE基因多态性与血清ACE水平有关,ACE水平依次为:DD型 >ⅠD型 >Ⅱ型,三者相互之间有显著性差异;原发性高血压并发脑梗死患者的D等位基因频率 (0. 64 )高于单纯EH组 ( 0 44 )和正常对照组 ( 0. 47 )。结论　当地人群基因多态性与血清ACE水平有关,ACE基因缺失多态性与高血压并发脑梗死有关,与高血压无明显相关。     

Gallium 67 citrate scanning and serum angiotensin converting enzyme levels in sarcoidosis

Gallium 67 citrate scans and serum angiotensin converting enzyme (ACE) levels were obtained in 54 patients with sarcoidosis and analyzed in relation to clinical manifestations. 67Ga scans were abnormal in 97% of patients with clinically active disease (n = 30) and in 71% of patients with inactive disease (n = 24). Serum ACE levels were abnormally high (2 standard deviations above the control mean) in 73% of patients with clinically active disease and in 54% of patients with inactive disease. Serum ACE levels correlated significantly with 67Ga uptake score (r =.436; p less than .005). The frequency of abnormal 67Ga scans and elevated serum ACE levels suggests that inflammatory activity with little or no clinical expression is common in sarcoidosis. Abnormal 67Ga scans were highly sensitive (97%) but had poor specificity (29%) to clinical disease activity. The accuracy of negative prediction of clinical activity by normal scans (87%) was better than the accuracy of positive prediction of clinical activity by abnormal scans (63%). 67Ga scans can be used to support the clinical identification of inactive sarcoidosis.     

慢性脑供血不足患者颈总动脉检测及高压氧对肱动脉内皮依赖性舒张功能影响的评价

目的:检测慢性脑供血不足(CCCI)患者颈总动脉并评价高压氧对其肱动脉内皮依赖性舒张功能(EDD)的影响.方法:用彩色多普勒超声检测62例患者颈总动脉内中膜厚度(IMT)和斑块情况,并分别于高压氧治疗前及治疗10d后检测肱动脉EDD值,同时测定其血清NO和ET水平.结果:与正常人群(0.65±0.12)mm比较,所有C...     

Endotoxin reduces specific pulmonary uptake of radiolabeled monoclonal antibody to angiotensin-converting enzyme.

The biodistribution of radiolabeled monoclonal antibody (Mab) to angiotensin-converting enzyme (ACE) was examined in normal and endotoxin-treated rats. Endotoxin administration at a dose of 4 mg/kg induced mild or middle pulmonary edema. The ACE activity in lung homogenate remained virtually unchanged, while the activity of serum ACE increased 15 hr after endotoxin infusion. In normal rats, anti-ACE Mab accumulates specifically in the lung after i.v. injection. Endotoxin injection induces reduction of specific pulmonary uptake of this antibody. Even in non-edematous endotoxemia, the accumulation of anti-ACE Mab antibody (Mab 9B9) decreased from 19.02 to 11.91% of ID/g of tissue without any change in accumulation of control nonspecific IgG. The antibody distribution in other organs and its blood level were almost the same as in the control. In a case of endotoxemia accompanied by increased microvascular permeability, the lung accumulation of Mab 9B9 was reduced to 9.17% of ID/g of tissue, while the accumulation of nonspecific IgG increased to 1.44% versus 0.89% in the control.     

No association between ACE I/D polymorphism and cardiovascular hemodynamics during exercise in young women

The ACE I/D polymorphism has been shown to interact with habitual physical activity levels in postmenopausal women to associate with submaximal and with maximal exercise hemodynamics. This investigation was designed to assess the potential relationships between ACE genotype and oxygen consumption (VO2), cardiac output (Q), stroke volume (SV), heart rate (HR), blood pressure (BP), total peripheral resistance (TPR), and arteriovenous oxygen difference ([a-v]O2 diff) during submaximal and maximal exercise in young sedentary and endurance-trained women. Seventy-seven 18-35-yr-old women underwent a maximal exercise test and a number of cardiac output tests on a treadmill using the acetylene rebreathing technique. ACE genotype was not significantly associated with VO2max (II 41.4+/-1.2, ID 39.8+/-0.9, DD 39.8+/-1.1 ml/kg/min, p=ns) or maximal HR (II 191+/-2, ID 191+/-1, DD 193+/-2 bpm, p=ns). In addition, systolic and diastolic BP, (a-v)O2 diff, TPR, SV, and Q during maximal exercise were not significantly associated with ACE genotype. During submaximal exercise, SBP, Q, SV, HR, TPR, and (a-v)O2 diff were not significantly associated with ACE genotype. However, the association between diastolic BP during submaximal exercise and ACE genotype approached significance (p=0.08). In addition, there were no statistically significant interactions between ACE genotype and habitual physical activity (PA) levels for any of the submaximal or the maximal exercise hemodynamic variables. We conclude that the ACE I/D polymorphism was not associated, independently or interacting with habitual PA levels, submaximal, or maximal cardiovascular hemodynamics in young women.     

模拟失重4周大鼠动脉血管局部肾素-血管紧张素系统表达的改变

目的 探讨局部肾素－血管紧张素系统（RAS）在模拟失重所致血管分化性适应中的作用。方法 大鼠通过尾部悬吊模拟失重，悬吊4周后，处死大鼠，分别取基底动脉，颈总动脉，腹主动脉和股动脉组织，提取总核糖核酸（RAN），用逆转录酶－多聚酶链式反应（RT－PCR），半定量检测各动脉组织局部RAS关键成份血管紧张素原（AGT）和血管紧张素转化酶（ACE）mRNA的表达水平，并通过脱氧核糖核酸（DNA）测定对PCR结果进行验证。结果 正常大鼠4种不同部位的动脉组织均有AGT和ACE基因表达；4周模拟失重后，悬吊组大鼠基底动脉AGT和ACEmRNA水平明显升高（P＜0．05），股动脉AGTmRNA水平下降（P＜0．05），其余两种血管组织则未见上述基因表达的明显变化。结论 生理条件下的大鼠基底动脉，颈总动脉，腹主动脉和股动脉均有局部RAS关键成份的表达；模拟失重后基底动脉和股动脉局部RAS表现出现了性质相反的变化，提示局部RAS很可能参与了模拟失重后动脉血管结构和功能的重塑。     

飞行员血管紧张素转换酶基因插入/缺失多态性及其血清水平的研究

目的了解飞行员血管紧张素转换酶(ACE)基因插入/缺失（I/D）多态性及其血清水平,探讨ACE基因多态性与飞行员耐力可能的关系。方法飞行员118例,健康对照者96例,用聚合酶链反应（PCR）扩增技术检测ACE基因I/D多态性,用比色法测定血清ACE水平。结果位于ACE基因第16内含子的I/D多态性经PCR扩增后呈三种基因型纯合子插入型（II）、纯合子缺失型（DD）和杂合子插入/缺失型（I/D）。飞行员组II基因型（44.07%）和Ⅰ等位基因频率（0.65）显著高于健康对照组(分别为31.25%和0.52)。ACE基因多态性与血清ACE水平明显相关(DD>ID,DD>II)。结论ACEⅠ基因有可能在飞行员的飞行耐力中起重要作用。