L—精氨酸对低氧性肺动脉高压大鼠肺动脉平滑肌细胞凋亡？…

目的 探讨Ｌ－精氨酸（Ｌ－Ａｒｇ）对低氧性肺动脉高压大鼠不同节段肺动脉平滑肌细胞凋亡的影响。方法 将Ｗｉｓｔａｒ大鼠（ｎ＝１９）随机分为对照组（ｎ＝７）、低氧组（ｎ＝６）及低氧＋Ｌ－Ａｒｇ组（ｎ＝６）。经右心导管法测定各组大鼠肺动脉压力和右室（ＲＶ）／左室＋室间隔（ＬＶ＋Ｓ）比值,以分光光度法间接测定血浆一氧化氮（ＮＯ）含量,通过ＴＵＮＥＬ法检测各组大鼠肺动脉压力和右室（ＲＶ）／左室＋室间隔（ＬＶ     

L—精氨酸对急慢性缺氧大鼠肺循环和脑血流的影响

研究了Ｌ－精氨酸（Ｌ－Ａｒｇ）对急慢性缺氧大鼠肺循环和脑血流的影响。一次注射Ｌ－Ａｒｇ４００ｍｇ．ｋｇ＾－＾１对急性缺氧性肺血管收缩反应（ＨＰＶ）无影响，而８００ｍｇ．ｋｇ＾－１有明显抑制作用；两种剂量的Ｌ－Ａｒｇ对缺氧性脑血流的变化均无显著影响。Ｌ－Ａｒｇ（３００ｍｇ．ｋｇ＾－＾１．ｄ＾－＾１）能缓解慢性缺氧性肺动脉高压，肺管阻力增高和右心肥厚，并抑制ＨＰＶ，但对脑血流无显著影响。ＮＯ合成酶抑制     

L－精氨酸对急慢性缺氧大鼠肺循环和脑血流的影响

研究了Ｌ－精氨酸（Ｌ－Ａｒｇ）对急慢性缺氧大鼠肺循环和脑血流的影响。一次注射Ｌ－Ａｒｇ４００ｍｇ·ｋｇ￣（－１）对急性缺氧性肺血管收缩反应（ＨＰＶ）无影响，而８００ｍｇ·ｋｇ￣（－１）有明显抑制作用；两种剂量的Ｌ－Ａｒｇ对缺氧性脑血流的变化均无显著影响。Ｌ－Ａｒｇ（３００ｍｇ·ｋｇ￣（－１）·ｄ￣（－１））能缓解慢性缺氧性肺动脉高压、肺血管阻力增高和右心肥厚，并抑制ＨＰＶ，但对脑血流无显著影响。ＮＯ合成酶抑制剂Ｌ－精氨酸甲酯可拮抗Ｌ－Ａｒｇ的作用，提示Ｌ－Ａｒｇ的作用可能与增加ＮＯ合成有关。     

钙通道阻滞剂及L—精氨酸对肺动脉高压的影响

采用常压间竭低氧模型，观察了钙通道拮抗剂尼群地平（Ｎｉｔ）、硝苯吡啶（Ｎｉｆ）、内皮依赖性血管舒张因子（ＥＤＲＦ）合成前体Ｌ－精氨酸（Ｌ－Ａ）对大鼠慢性低氧性肺动脉高压的预防作用。结果提示：三者均能预防低氧性肺动脉高压形成和减轻低氧引起的右室肥大：Ｎｉｔ、Ｎｉｆ与Ｌ－Ａ比较无显著性差异（Ｐ＞０．０５）；Ｎｉｔ对低氧性肺动脉高压的降压作用较Ｎｉｆ稍好。     

L—精氨酸对高血压的防治作用

Ｌ－精氨酸通过ＮＯ的释放增加参与神经内分泌，血管活性物质等的调节；动物实验和高血压病人资料显示：Ｌ－精氨酸具有抗高血压的作用，因而在某种条件下可作药用。     

钙通道阻滞剂及L－精氨酸对肺动脉高压的影响

采用常压间竭低氧模型，观察了钙通道拮抗剂尼群地平（Ｎｉｔ）、硝苯吡啶（Ｎｉｆ）、内皮依赖性血管舒张因子（ＥＤＲＦ）合成前体Ｌ－精氨酸（Ｌ－Ａ）对大鼠慢性低氧性肺动脉高压的预防作用。结果提示：三者均能预防低氧性肺动脉高压形成和减轻低氧引起的右室肥大；Ｎｉｔ、Ｎｉｆ与Ｌ－Ａ比较无显著性差异（Ｐ＞０．０５）；Ｎｉｔ对低氧性肺动脉高压的降压作用较Ｎｉｆ稍好。     

洛沙坦对蛋白激酶C在慢性缺氧大鼠模型肺动脉胶原表达作用的影响

目的　观察洛沙坦对蛋白激酶C(PKC)在慢性缺氧大鼠模型肺动脉胶原表达作用的影响。方法　将二级SD大鼠分为 3组 :A组 (正常对照组 )大鼠室内常规饲养。B组 (单纯缺氧 4周组 )大鼠置于常压低氧舱中 ,舱内充入氮气 ,使氧浓度维持在 (1 0 0± 0 5) % ,每天 8h ,每周 6d ,连续 4周 ;大鼠每天缺氧前用 2ml蒸馏水灌胃。C组 (洛沙坦干预组 )缺氧条件同B组 ,大鼠每天缺氧前用洛沙坦 (洛沙坦 50mg/kg溶于 2ml蒸馏水 )灌胃。采用透射电镜、放射活性测定法、免疫组化、原位杂交等方法观察 3组大鼠肺细小动脉超微结构、肺组织PKC活性、肺动脉管壁PKC免疫组化及Ⅰ、Ⅲ型胶原和Ⅰ、Ⅲ型前胶原基因表达的变化。结果　 (1 )B组大鼠平均肺动脉压、右心室重量比显著高于A组(P <0 0 1 ) ,C组显著低于B组 (P <0 0 1 )。 (2 )光镜下可见B组大鼠肺血管管壁厚度占血管外经的百分比、管壁面积占管总面积的百分比显著高于A组 (P <0 0 1 ) ,C组显著低于B组 (P <0 0 1 )。电镜下可见B组大鼠肺动脉胶原纤维较A组明显为多 ,C组较B组明显为少。 (3)B组大鼠肺组织细胞PKC总活性、胞膜PKC活性、胞质PKC活性及胞膜PKC活性占PKC总活性的百分比显著高于A组(P <0 0 1 ) ,C组上述指标均显著低于B组 (P <0 0 1 )。 (4)免疫组化显示 ,B     

L—精氨酸对培养心肌细胞氧自由基损伤的影响

<正> 近年来许多研究表明,一氧化氮(NO)是一个重要的细胞内信使,具有多种生理作用,尤其在心血管系统中,NO的生物学效应具有非常重要的意义,涉及到许多生理病理过程,有关NO对心脏、血管的生物调节作用已有大量的研究,而NO在氧自由基损伤过程中起何种作用尚不很清楚.目前尚无一致的意见,我们使用培养的心肌细胞观察NO前体L—精氨酸对氧自由基致损心肌细胞的影响.探讨NO的某些作用机理.     

L—精氨酸对肾性高血压心肌肥厚大鼠左室超微结构的影响

目的 观察L－精氨酸（L－Arg)对血管性高血压心肌肥厚大鼠左室肌超微结构的影响。方法 L－Arg治疗高血压心肌肥厚大鼠8周后处死,镜检左室心肌亚细胞结构改变。结果 经8周治疗后可见L－Arg治疗组心肌细胞肌丝排列整齐、核规则、核仁清晰、线粒体形态结构正常。结论 L－Arg能有效保护心肌亚细胞结构。     

L-精氨酸对肺血栓栓塞症eNOS和COX2表达的影响

目的观察L-精氨酸（L-Arg）对实验性肺血栓栓塞症（PTE）中内皮型一氧化氮合酶（eNOS）及环氧合酶2（COX2）的影响．探讨其对PTE的作用机制。方法采用自体血栓回输的方法制备PTE大鼠模型．L-Arg组经腹腔注射L-Arg 100mg／kg。用免疫组化和RT-PCR技术检测肺组织eNOS和GOX2 mRNA和蛋白表达。结果肺栓塞后病理可见肺动脉血栓形成,炎性反应明显。与模型组比较。L-Arg组肺组织病变程度减轻,eNOS mRNA和蛋白表达上调,COX2 mRNA和蛋白表达下调。结论PTE时,L-Arg可通过下调肺内eNOS表达和上调COX2表达起到保护肺组织的作用。     

L-精氨酸对慢性阻塞性肺病营养支持增效作用的探讨

目的:评价L-精氨酸对慢性阻塞性肺病(COPD)营养支持的增效作用。方法:对30例COPD患者进行营养支持治疗，总能量摄入为静息能量消耗(REE)的1．5倍，其中蛋白质占20％，脂肪30％，碳水化合物50％。12例为精氨酸治疗组，口服L-精氨酸10g，每天3次，18例为对照组，观察效果。结果:营养支持后，精氨酸组肱三头肌皮褶厚度、前白蛋白、体脂等营养参数较对照组明显改善，呼吸肌力显著提高，REE显著下降。结论:L-精氨酸不仅改善COPD的营养状况和呼吸肌力量，而且能显著降低患者的能量消耗，强化营养支持的效果，改善预后。     

吸氧对慢性缺氧高二氧化碳大鼠肺血管L-精氨酸转运的影响

目的　探讨慢性缺氧 (O2 )高二氧化碳 (CO2 )对大鼠肺动脉L 精氨酸 (L Arg)转运的影响与吸氧的作用。方法　将 4 0只大鼠以随机区组设计法分成 4组 ,用 0 2mmol/L和 5 0mmol/L [3 H] Arg将肺动脉孵育 ,测定其对 [3 H] L Arg的摄取率、一氧化氮合酶 (NOS)活性与一氧化氮 (NO2 /NO3)含量。每组 1 0只。正常对照组 (A组 )、慢性缺O2 4周后伴高CO2 4周组 (B组 )、慢性缺O2 4周伴高CO24周后吸空气 4周组 (C组 )及慢性缺O2 4周伴高CO2 4周后吸O2 4周组 (D组 )。结果　 (1 )肺动脉平均压 (mPAP)、右心室 (RV)和左心室 +室间隔 (LV +S)重量比值 (RV/LV +S) :B组 (33% )与A组(35 % )比较差异有显著性 (P均 <0 0 1 ) ;D组 (2 4 % )与C组 (2 4 % )比较 ,差异也有显著性 (P均 <0 0 5 )。 (2 )离体孵育的肺动脉摄取低浓度 (0 2mmol/L)和高浓度 (5 0mmol/L) [3 H] L Arg比较 :B组分别为 [(3 0 4± 0 1 6 ) μmol·g-1 min-1 ]、[(8 1 2± 0 1 4 ) μmol·g-1 ·min-1 ],A组分别为 [(4 6 2± 0 5 5 )μmol·g-1 ·min-1 ]、[(1 1 2 4± 1 0 2 ) μmol·g-1 ·min-1 ],A、B两组比较差异有显著性 (P均 <0 0 1 ) ;而D组分别为 [(4 30± 0 1 8) μmol·g-1 ·min-1 ]、[(1 2 31± 0 6 5 ) μmol·g-1 ·m     

波生坦对低氧性肺动脉高压大鼠肺动脉钙调节蛋白表达的影响

目的: 探讨波生坦（bosentan,BST）对低氧性肺动脉高压（HPH）大鼠肺动脉中钙调节蛋白（calponin,CPN）表达的影响。 方法: 40只健康SD大鼠随机分为正常组、模型组、安慰剂组和BST组,每组各10只。正常组常压常氧下饲养6周,其他组分别置于全自动调节的低压低氧仓中间断低氧(8 h/d),分别饲养3周、6周和6周。自第4周起,模型组常压常氧下饲养;安慰剂组和BST组大鼠在入仓前分别给予生理盐水（2 ml）和BST（100 mg/kg）灌胃。以6周为观察终点,经HE染色后,观察各组大鼠肺血管的形态学变化;应用图像采集处理系统检测各组大鼠中型及小型肺动脉的相对中膜厚度(RMT);用免疫组化染色法对各组大鼠肺动脉的CPN进行定位及半定量分析。结果: ①与其他组相比,安慰剂组大鼠肺动脉管壁增厚、管腔狭窄;BST组大鼠肺动脉管壁的厚度及管腔大小可恢复至正常组的状态;②各组大鼠肺动脉管壁中均有CPN表达,随着低氧时间的延长,CPN表达减少,BST组CPN表达与正常组相比无统计学差异。结论: BST可促进HPH大鼠肺动脉CPN的合成。     

Effect of chinonin on acute hypoxic pulmonary vasoconstriction in Sprague-Dawley rats

Abstract The objective of this study was to determine the influence of chinonin on acute hypoxic pulmonary vasoconstriction (HPV) in Sprague-Dawley (SD) rats and investigate its mechanism. Sixty-five SD rats were divided into five groups at random: six in the control group; six in the hypoxia group; 13 in the group of hypoxia with chinonin; 20 in the group of endothelin-1(ET-1) with chinonin and 20 in the group of platelet activating factor (PAF) with chinonin. Their mean pulmonary arterial pressures (mPAP) were measured and the concentration of molondialdehyde (MDA) in plasma and the activity of phospholipase A₂ (PLA₂) of the lung tissues were detected. The PAF and ET-1 levels of plasma and lung homogenates were detected in the control and hypoxia groups. There was evidence of an increase in mPAP, MDA, PAF and ET-1 in the plasma, and activity of PLA₂, PAF and ET-1 of the lung tissues when the rats inhaled a 10% mixture of oxygen in nitrogen. It appeared that chinonin may have been inhibiting the action of ET-1 and PAF. Chinonin could have prevented an increase in MPAP caused by hypoxia and inhibited the action of ET-1 and PAF. But chinonin had no influence on the increase in MDA in the plasma and the PLA₂ activity of the lungs when hypoxia occurred. Chinonin can reduce HPV, but does not influence normal mPAP. It may do this by blocking the action of ET-1 and/or PAF or others. The definite mechanism needs to be studied further.     

Intravascular ultrasound imaging of the pulmonary arteries in primary pulmonary hypertension

OBJECTIVE: Intravascular ultrasound has the unique ability to provide cross-sectional images of the arterial wall. This study examined intravascular ultrasound (IVUS) images of the proximal pulmonary arteries in primary pulmonary hypertension (PPH). METHODOLOGY: Study 1: Specimens from four patients who had died of PPH (in vitro PPH group) were compared with those of three patients who had died of subarachnoid haemorrhage but had no evidence of cardiopulmonary disease (in vitro control group). Three-centimetre segments of the following levels were examined by IVUS: pulmonary trunk, eight secondary branch arteries of the upper, middle, and lower lobes of both lungs, and the thoracic descending aorta. Study 2: Four patients with PPH (in vivo PPH group) and five patients without pulmonary hypertension and no evidence of cardiopulmonary disease (in vivo control group) were examined. The IVUS images of the apical segmental artery of the right upper lobe and the descending branch of the right pulmonary artery were studied. RESULTS: Echographic examination of formalin-fixed preparations of secondary branch sections of the pulmonary artery failed to show a clear three-layer structure in the in vitro control group (24 preparations), but a distinct three-layer structure and increased vessel wall thickness were observed in the in vitro PPH group (32 preparations). Similar findings were obtained in the in vivo study. The mean echo density of the proximal pulmonary arterial wall correlated well with the mean pulmonary arterial pressure (mPA) in the in vitro PPH, and also correlated with the mPA in the in vivo study (r = 0.960, P < 0.0001). The echo intensity of secondary branch sections of the pulmonary artery was higher in the in vitro PPH group than in the in vitro control group (180.5 +/- 27.0 vs 132.5 +/- 26.7 counts, P < 0.001); similar results were obtained in the in vivo study (144.7 +/- 23.4 vs 85.0 +/- 14.3 counts, P < 0.01). CONCLUSIONS: These results suggest that the histological changes detected in the pulmonary artery walls in the PPH group were responsible for the increased echo intensity.     

缺氧性腺泡内肺动脉构形重组的形态定量研究

目的观察中药黄芪对缺氧性肺动脉高压及肺腺泡内动脉结构改建的抑制作用。方法６０只大白鼠随机分成缺氧组、缺氧＋黄芪组、正常对照组（各组２０只）。缺氧组、缺氧＋黄芪组大鼠在常压缺氧（１０％Ｏ２１０小时／天）下喂养，在实验第１５天、３０天每组分别取１０只进行右心室收缩压、右心室肥大指数测定后处死，再对肺腺泡内动脉进行光镜、电镜观察及形态学定量分析。结果在实验第３０天后，右心室收缩压，在缺氧组高于缺氧＋黄芪组１８倍（Ｐ＜０．０５），右心室肥大指数，在缺氧组高于缺氧＋黄芪组１３倍（Ｐ＜０．０５），腺泡内动脉中层厚度高于缺氧＋黄芪组２３倍（Ｐ＜０．０５）；肺腺泡内动脉外膜单位面积的纤维母细胞数（密度）在缺氧组是１３１±０３（Ｐ＜０．０５），在缺氧＋黄芪组是７６０±０１９（Ｐ＜０．０５）。结论黄芪抑制了肺腺泡内动脉壁细胞增生及扩张肺动脉，黄芪在抑制肺动脉高压结构改建中可能起重要作用     

新型内源性气体信号分子硫化氢对低氧性肺血管胶原重塑的影响

目的研究大鼠低氧性肺血管重塑时硫化氢(H2S)对Ⅰ、Ⅲ型胶原蛋白在肺血管壁异常堆积的调节作用,进一步探讨H2S缓解低氧性肺血管重塑的作用机制。方法19只雄性Wistar大鼠随机分为对照组、低氧组、低氧+硫氢化钠(NaHS)组。低氧组和低氧+NaHS组大鼠共低氧21d,低氧+NaHS组大鼠每天低氧前腹腔注射H2S供体NaHS。低氧结束后,测定肺动脉平均压(mPAP),称重右心室(RV)和左心室+室间隔(LV+SP),计算RV/(LV+SP)。亚甲蓝分光光度法测定血浆中H2S含量。免疫组化染色检测Ⅰ、Ⅲ型胶原蛋白,原位杂交检测Ⅰ、Ⅲ型前胶原mRNA在肺血管壁表达。结果(1)与对照组相比,低氧组大鼠mPAP升高46%,RV/(LV+SP)增加41%,血浆H2S含量下降36%(P均<0·01);与低氧组相比,低氧+NaHS组大鼠的mPAP降低31%,RV/(LV+SP)减少24%,血浆H2S含量升高65%(P均<0·01)。(2)各组大鼠肺小型、中型肌性动脉中Ⅰ型胶原蛋白表达的比较:低氧组较对照组分别增加81%、62%(P<0·01);低氧+NaHS组较低氧组分别减少了32%、18%(P<0·01)。(3)各组大鼠肺小型、中型肌性动脉中Ⅰ型前胶原mRNA表达的比较:低氧组较对照组分别增加49%、68%(P<0·01);低氧+NaHS组较低氧组分别减少了31%、33%(P<0·01)。(4)各组大鼠肺小型肌性动脉中Ⅲ型胶原蛋白表达的比较:低氧组较对照组增加84%(P<0·01);低氧+NaHS组较低氧组减少了37%(P<0·01)。低氧组大鼠的肺中型肌性动脉中Ⅲ型胶原蛋白表达较对照组增加38%(P<0·01);但是与低氧+NaHS组相比无明显变化(P>0·05)。(5)各组大鼠肺小型、中型肌性动脉中Ⅲ型前胶原mRNA表达的比较:低氧组较对照组分别增加53%、17%(P<0·01);低氧+NaHS组较低氧组分别减少了45%、33%(P<0·01)。结论在大鼠低氧性肺血管胶原重塑时,H2S能够抑制Ⅰ、Ⅲ型胶原蛋白及其mRNA在肺血管壁的表达,此作用可能是其缓解低氧性肺血管重塑的作用机制之一。     

Clinical evaluation of serum type IV collagen 7S in idiopathic pulmonary fibrosis

Abstract Type IV collagen is one of the major components of the basement membrane (BM). 7S domain (7S collagen) of type IV collagen is an N-terminal peptide which is stable against protease and heat. We investigated serum concentration of 7S collagen in patients with idiopathic pulmonary fibrosis (IPF) and other pulmonary diseases. The aim of this study was to evaluate whether changes in the serum concentration of 7S collagen reflect the fibrotic process of IPF. We measured the concentration of serum 7S collagen with radioimmunoassay in patients with IPF, chronic pulmonary emphysema (CPE), sarcoidosis, infectious pulmonary diseases (IPD) and normal healthy controls. We also monitored 7S collagen during the clinical course in some patients with IPF and investigated the correlation between the serum 7S collagen, and lactate dehydrogenase (LDH) and erthrocyte sedimentation rate (ESR) in patients with IPF. Patients with IPF showed significantly higher serum concentration of 7S collagen than other pulmonary diseases and healthy controls. The serum concentration of 7S collagen significantly decreased in IPF patients who showed roentgenographic improvement after corticosteroid treatment. There was a correlation between the serum 7S collagen and LDH, and ESR. In conclusion, serum concentrations of 7S collagen increase in patients with IPE The measurement of 7S collagen is useful for the evaluation of fibrotic change in the lung.     

Use of small stents for rehabilitation of hypoplastic pulmonary arteries in pulmonary atresia with ventricular septal defect.

Branch pulmonary artery stenosis frequently occurs in pulmonary atresia with ventricular septal defect (PA/VSD). Balloon dilation alone is often unsuccessful in patients with severely hypoplastic pulmonary arteries with residual stenoses after surgical repair. In an attempt to promote distal pulmonary artery growth, 17 stents were placed in 12 severely stenotic pulmonary artery lesions in 10 patients with PA/VSD. All had prior surgery, including pulmonary artery repair, right ventricle to pulmonary artery homograft, and, in 6 of 10, closure of VSD. Median age at stent placement was 16.8 months (range, 13.2-56). Stents were placed using 3.0, 3.5, or 4.0 mm balloons in all but one lesion, in which a 7 mm balloon was used. Following stent placement, there was an increase in the lesion diameter from 1.5 to 3.4 mm (P < 0.05) and an increase in flow to the affected lung from 27% to 34% (P < 0.05). Repeat catheterization 2 to 6 months after stenting in six patients revealed complete occlusion in two of eight lesions. In the other six vessels, there was an increase in distal vessel diameter from 2.96 to 3.94 mm (P < 0.05) even though four had severe restenosis requiring restenting. Two patients underwent surgical pulmonary artery reconstruction and stent removal because of adequate distal vessel growth. Stenting of hypoplastic pulmonary arteries in PA/VSD results in immediate improvement in vessel size and blood flow. Stent restenosis is common although distal vessel growth can be achieved. Stenting of these lesions should be reserved only for those patients unresponsive to other interventions.