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1.
EffectofElectroacupunctureonPulmonaryβ-AdrenoceptorinAllergicAsthmaGuinea-PigsLaiXin-sheng(赖新生),XuMin(徐敏)(GuangzhouUniversity...  相似文献   

2.
EfficacyofFructusBruceaeEmulsionwithChemotherapyinTreatmentofAdvancedPulmonaryCarcinomaSUNKai(孙慨);WEIGui-zhen(魏桂珍)andWANGYa-x...  相似文献   

3.
ObservationofthePreventiveandTherapeuticEffectofChuanxiongontheAtherosclerosisofRabbitsWangJing(王京),LiuXue-ru(刘雪如)(GeneralNav...  相似文献   

4.
RefinedRhubarbTabletsintheTreatmentofAcuteHemorrhagingoftheUpperDigestiveTractJiaoDong-hai(焦东海);ZhuZong-wei(朱宗巍);GanZi-cheng(...  相似文献   

5.
LaparoscopyintheDiagnosisandtheTreatmentofInfertility(Analysisof340consecutivecases)¥(葛春晓,刘梦梅,丁慧娟,曹雪芬)GeChum-xiao;LiuMeng-mei...  相似文献   

6.
Complicatedmodulatingmechanismsareinvolvedinthenetworkbetweenner-vousandimmunesystem.Interleukin-1(IL-1),asanimportantcytokin...  相似文献   

7.
EffectoftheExtractsofPumpkinSeedsontheUrodynamicsofRabbits:AnExperimentalStudyZHANGXu(张旭),OuyangJin-zhi(欧阳金芝),ZHANGYong-shang...  相似文献   

8.
AStudyoftheMechanismofYinzhihuang(菌栀黄)InjectionintheTreatmentofInfantileHepatitisSyndromeDongYong-sui(董永绥);HuangZhi-hua(黄志华);...  相似文献   

9.
TheEffectofLigationofPortalBranchontheGrowthofImplantedTumoroftheLiverinRatsBAIZhi-jun(白植军),FENGXian-song(冯贤松)(DepartmentofSu...  相似文献   

10.
EffectsofAngelicaeSinensisonOxygenFreeRadicalsandProslaglandinsinPatienteofChronicPulmonaryHeartDiseaseXuJun-yang(许军阳);ZhouZh...  相似文献   

11.
肺动脉高压形成机制中的气体信号分子网络   总被引:9,自引:1,他引:8  
目的:肺动脉高压的形成机制至今还不清楚.近年来我们围绕气体信号一氧化氮及一氧化碳调节网络在肺动脉高压形成机制中的作用开展了系列研究.方法:低氧性肺动脉高压及高肺血流性肺动脉高压动物模型的建立,血流动力学测定,血管环舒张反应研究,肺动脉超微及显微结构研究,分子生物学,免疫细胞化学,免疫组织化学,流式细胞术,生物化学,肺动脉平滑肌细胞及内皮细胞培养等.结果:一氧化氮、一氧化碳及其调节网络在肺血管结构重建、肺动脉高压形成中发挥重要作用.二者参与对肺动脉平滑肌细胞增殖的抑制作用及凋亡的促进作用,证明二者对肺动脉高压时胶原堆积具有抑制作用.研究同时发现,二者对平滑肌细胞增殖促进因子的抑制作用以及对平滑肌细胞增殖抑制因子的促进作用参与其对肺血管结构重建、肺动脉高压形成的调节.结论:一氧化氮、一氧化碳及其调节网络在肺动脉高压的形成中发挥重要作用.  相似文献   

12.
Summary The monocrofaline-induced structural changes of small pulmonary arteries in rat and their relationship with pulmonary hypertension and right ventricular hypertrophy were observed by determining the right ventricular systolic pressure, and by light and electron microscope and morphometry. One to 38 days after last injection of monocrotaline (MCT), a medial thickening and lumen marrrowing of the circular muscular arteries (CMA), accompanying terminal (TB) and respiratory bronchioles (RB), were found. And there after the lumen of CMA, accompanying TB, became dilated, and its medial thickness (MT) decreased, whereas the histopathologic changes of the partially muscular arteries (PMA), accompanying RB, became severe, their MT increased continuously, and finally reached the peak value on Day 50. At the first day after last MCT treatment, inflammation and muscularization were found in PMA and nonmuscular arteries (NMA), and became more severe with the cause of disease. Therefore, the intra-acinar pulmonary arteries, both CMA and PMA, increased in number while the NMA decreased in number significantly because of the structural remodeling. Four days after MCT treatment, the right ventricular systolic pressure began to rise, and reached its peak value on Day 50. Eight days after MCT injection, right ventricular hypertrophy developed, and became most significant from Day 23 to Day 30. The results suggest that structural remodeling, i.e. muscularization, of intra-acinar pulmonary arteries plays an important role in the development of pulmonary hypertension and right ventricular hypertrophy.  相似文献   

13.
目的:探讨高肺血流量所致肺动脉高压大鼠肺血管结构和内源性硫化氢体系的变化。方法:SD大鼠共16只,随机分为分流组及对照组。对分流组大鼠行腹主动脉—下腔静脉分流术。11周后以右心导管法测定肺动脉平均压(pulmonary artery mean pressure,mPAP)。检测右心室/体重(right ventricle/body weight,RV/BW)和右心室/左心室 室间隔(right ventricle/left ventricle plus septum,RV/LV S)比值。并且以光学显微镜和电子显微镜观测肺血管结构的变化。以分光光度法测定血浆硫化氢(hydrogen sulfide,H2S)含量。化学法测定肺组织硫化氢产出率,以原位杂交的方法检测肺动脉胱硫醚—γ—裂解酶(cystuthionine—γ—lyase,CSE)mRNA表达。结果:分流组大鼠mPAP、RV/BW及RV/(LV S)比值明显高于对照组,光镜下肺小血管肌化程度明显增强,肺中、小肌型动脉相对中膜厚度明显增加。电镜下,肺中、小肌型动脉内皮细胞增生、肥厚、肿胀,平滑肌细胞增生、肥厚,并由收缩表型向合成表型转化。分流组大鼠的血浆H2S含量及肺组织CSE活性(肺组织H2S产出率)明显低于对照组,肺动脉mRNA表达明显降低。结论:肺血管结构重建是高肺血流量所致肺动脉高压的重要病理基础,内源性H2S体系——mRNA表达、CSE活性及血浆H2S含量下降可能在其形成中起重要的作用。  相似文献   

14.
Alleviation of hypoxic pulmonary vascular structural remodeling by L-arginine   总被引:12,自引:1,他引:11  
目的探讨L-精氨酸(L-Arg)对低氧性肺血管结构重建的干预作用及其可能机制.方法将18只Wistar大鼠配伍后随机分为对照组、低氧组和低氧+L-Arg组(共6个配伍组).以右心导管法测定肺动脉压力,并对大鼠肺组织标本进行显微结构观测和超微结构观察,同时以分光光度法测定血浆一氧化氮(NO)含量,并对肺组织以内皮素-1(ET-1) cRNA探针进行原位杂交,研究肺动脉内皮细胞ET-1 mRNA的表达.结果低氧组大鼠肺动脉平均压明显高于对照组(20.33±2.18?mm?Hg vs 15.38±1.05?mm?Hg, P<0.05).低氧后大鼠肺血管显微及超微结构发生明显改变,肺血管结构重建形成.同时低氧组大鼠血浆NO间接含量明显低于对照组 (P<0.05 ).低氧后肺动脉内皮细胞ET-1 mRNA表达明显增强.然而,低氧+L-Arg组大鼠PAMP较低氧组明显降低(16.73±1.35?mm?Hg vs 20.33±2.18?mm?Hg, P<0.05).L-Arg缓解了低氧性肺血管结构重建的形成.同时低氧+L-Arg组大鼠血浆NO间接含量明显高于低氧组(P<0.05).L-Arg使低氧大鼠肺动脉内皮细胞ET-1 mRNA表达明显受抑制.结论 L-Arg对低氧性肺血管结构重建以及低氧性肺动脉高压的形成有重要的调节作用,其机制可能与通过促进低氧大鼠体内NO生成,从而抑制肺动脉内皮细胞ET-1 mRNA表达有一定的关系.  相似文献   

15.
(席思川)(车东媛)(张婉蓉)TheInhibitoryEffectofRadixSalviaeMiltiorrhizaeonHypoxicStructuralRemodelingofIntra-acinarPulmonaryArteries¥XISi-c...  相似文献   

16.
Summary In order to study the cellular origin of muscularization in non-muscular arterioles of the lung, the pulmonary vascular pericytes-culture was established. The terminal lung tissue of the rat was taken out and minced. Then 0.5 % of type IV collagenase solution was added for digestion and the microvascular segments were obtained by screening. The targeted cells were cultured by “selective conditioned media”. Under phase-contrast microscope, the cultured cells were large in size with ragged margin and numerous pseudopodia, which imparted tubule-like structure. There was no contact inhibition in growing cells, so multiple layers developed. When they were confluent, there were morphologically no “hillock and dale” growth pattern as in smooth muscle cells or “weave-like” pattern as in fibroblasts. The ultrastructure of cultured cells showed numerous digital processes, moderate amount of rough and smooth endoplasmic reticulum, rich Golgi’s apparatus, microfilaments, few lysosomes without myofilaments and dense bodies. Immunohistochemical staining revealed that the cultured pericytes had same kind of cellular skeletal protein, α-SM-actin, like smooth muscle cells. The cultured cells also exhibited positive reaction to CD34 antigen and S-100 antigen, which were negative in smooth muscle cells and fibroblasts. The cell growth pattern, ultrastructure and immunological phenotype suggested that the cultured cells had characteristics of vascular pericytes. Pericytes are one of the components of microvascular cells, and the establishment ofin vitro culture technique of pericytes is of significance for further exploration of the muscularization of non-muscular arterioles in lung and the mechanism of structural remodeling of pulmonary vessels. This project was supported by the grant of National Nature Sciences Foundation of China (No. 39570289).  相似文献   

17.
目的:探讨肾上腺髓质素1-50(ADM1-50)对大鼠慢性低氧性肺动脉高压和肺血管结构重建的作用及其机制.方法:20只雄性Wistar大鼠随机分为对照组(n=7)、低氧组(n=6)和低氧 ADM1-50组(n=7).对于低氧 ADMi-50组大鼠,通过皮下埋放微量渗透泵持续给予ADM1-50(300ng/h).低氧饲养2周后,以右心导管法测定肺动脉平均压(mPAP),检测右心室与左心室加室间隔的比值[RV/(LV S)],观测肺血管显微和超微结构的变化,以硝酸还原酶法测定血浆一氧化氮(NO)含量,以敏感硫电极法测量大鼠血浆中硫化氢(H2S)含量.结果:低氧2周后大鼠mPAP较对照组明显增高[(24.9±6.8)mmHg vs(14.3±2.4)mmHg,P<0.01,1 mmHg=0.133 kPa];RV/(LV S)也较对照组明显增高[(0.318±0.054)vs(0.182±0.007],P<0.01).肺动脉显微和超微结构发生明显改变.低氧组大鼠血浆NO和H2S含量明显低于对照组.低氧 ADM1-50组大鼠mPAP明显低于低氧组大鼠[(14.9±3.0)mmHg vs(24.9±6.8)mmHg,P<0.01];RV/(LV S)也明显低于低氧组[(0.185±0.011)vs(0.318±0.054),P<0.01].ADMi-50使低氧大鼠血浆NO和H2S的含量明显升高.结论:ADM1-50可能通过促进低氧大鼠体内NO和H2S的生成,对低氧性肺动脉高压和肺血管结构重建的形成发挥调节作用.  相似文献   

18.
低氧性肺动脉高压大鼠肺动脉和右心室重构研究   总被引:2,自引:0,他引:2  
目的研究慢性低氧对大鼠肺动脉血管和右心室重构的影响。方法常压间断低氧法复制大鼠慢性低氧模型。右心导管法测平均肺动脉压(mPAP);测平均主动脉压(mAP),血细胞比容(HCT);常规HE染色及右心室肥大指数(RVHI)研究右心室重构观察肺血管重构情况;结果慢性低氧大鼠(28d)血细胞比容和平均肺动脉压力显著升高。发生肺动脉血管重构,右心室肥大指数显著增加。结论慢性低氧化导致大鼠肺动脉压增高的同时,伴肺小动脉管壁增厚、管腔狭窄和右心室肥厚等重构性改变。  相似文献   

19.
L-精氨酸干预低氧性肺血管结构重构机制的研究   总被引:20,自引:0,他引:20  
探讨L-精氨酸干预低氧性肺血管结构重构的机制。方法将18只Wistar大鼠采用区组随机法分为对照组、低氧组和低氧+L-Arg组。以右心导管法测定肺动脉压力,并对大示本进行显微结构观测和超微结构观察,同时分光光度法间接测定血浆一氧化氮(NO)含量,并对肺组织以内皮素-1(ET-1)cRNA探针进行原位杂交,研究肺动脉内皮细胞ET-1mRNA的表达。结果低氧组大鼠肺动脉平均压(mPAP)为2.71KP  相似文献   

20.
目的:探讨L-精氨酸(L-arginine,L-Arg)对低氧性肺血管结构重建大鼠肺动脉平滑肌细胞凋亡的影响及其机制.方法:将17只Wistar大鼠随机分为对照组(n=7)、低氧组(n=5)和低氧+L-Arg组(n=5).对大鼠肺血管进行显微形态学观测.通过末端转移酶介导的dUTP切口末端标记法(TUNEL)检测肺动脉平滑肌细胞凋亡,并以免疫组织化学方法研究肺动脉平滑肌细胞Fas表达.结果:低氧2周后出现大鼠肺血管结构重建.同时,肺中、小型动脉凋亡平滑肌细胞百分数均明显低于对照组(P均<0.05),平滑肌细胞Fas表达明显降低.然而,L-Arg缓解了低氧性肺血管结构重建的形成.低氧+L-Arg组大鼠肺中、小型动脉凋亡平滑肌细胞百分数均明显高于低氧组(P均<0.05).L-Arg使低氧大鼠肺动脉平滑肌细胞Fas表达明显增强.结论:L-Arg通过使肺动脉平滑肌细胞Fas表达上调,促进肺动脉平滑肌细胞的凋亡,从而对低氧性肺血管结构重建有重要的调节作用.  相似文献   

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