缺氧大鼠肺组织氧化／抗氧化平衡的变化及其与TXA2／PGI2平…

检测缺氧大鼠肺组织丙二醛，超氧化物歧化酶和过氧化氢酶含量以及血浆ＴＸＡ２和ＰＧＩ２浓度，以探讨氧自由基及ＴＸＡ２－ＰＧＩ２在缺氧性肺动脉高压中的作用。结果表明：与对照组比较缺氧大鼠肺组织ＭＤＡ明显升高、ＳＯＤ、ＣＡＴ明显降低，ＶｉｔＥ可逆转ＭＤＡ和ＳＯＤ的变化。     

慢性阻塞性肺病患者血浆血栓素B_2和6－酮－前列腺素F_（1α）含量的变化及其与肺动脉高压的关系

为了探讨慢性阻塞性肺病（ＣＯＰＤ）患者血栓素Ａ_２（ＴＸＡ_２）和前列环素（ＰＧＩ_２）与肺动脉高压的关系，我们对伴有和不伴有肺动脉高压的３０例缓解期ＣＯＰＤ患者血浆中血栓素Ｂ_２（ＴＸＢ_２）及６－酮－前列腺素Ｆ_（１α）（６－ｋｅｔｏ－ＰＧＦ_（１α））的含量变化进行了观察，还对７例伴肺动脉高压的ＣＯＰＤ患者不同病期的肺动脉平均压（ＰａＰ）、血浆ＴＸＢ_２及６－ｋｅｔｏ－ＰＧＦ_（１α）．水平作了对比分析。结果发现，缓解期ＣＯＰＤ患者中，伴肺动脉高压者血浆ＴＸＢ_２明显增高，６－ｋｅｔｏ－ＰＧＦ_（１α）显著下降，ＴＸＢ_２／６－ｋｅｔｏ－ＰＧＦ_（１α）明显增大，与不伴肺动脉高压者比较，差异非常显著（Ｐ均＜０．０１），而不伴肺动脉高压者的这些指标与正常人的比较，则无统计学意义（Ｐ均＞０．０５）；与急性期比较，ＣＯＰＤ患者缓解期ＰａＰ明显下降，ＴＸＢ_２亦显著降低，６－ｋｅｔｏ－ＰＧＦ_（１α）明显升高，ＴＸＢ_２／６－ｋｅｔｏ－ＰＧＦ_（１α）缩小（Ｐ均＜０．０１）；相关分析发现，伴肺动脉高压者ＰａＰ与ＴＸＢ_２呈明显正相关，与６－ｋｅｔｏ－ＰＧＦ_（１α）呈负相关（ｎ＝２８，ｒ＝＋０．４６、－０．３９，Ｐ均＜０．０５）     

常压缺氧大鼠血浆和肺组织TXB_2和6－keto－PGF_（1α）的动态变化

本文观察常压缺氧２４ｈ及１，２，４ｗ（６ｈ／ｄ，６ｄ／ｗ）后大鼠血小板数及聚集率和血浆及肺ＴＸＢ＿２和６－ｋｅｔｏ－ＰＧＦ＿（１α）的动态变化。结果表明（１）缺氧大鼠血小板数呈先增加、后恢复、再下降，血小板聚集率呈先减少、后增加再减少的动态变化。（２）血浆ＴＸＢ＿２和６－ｋｅｔｏ－ＰＧＦ＿（１α）均明显升高，（３）肺组织６－ｋｅｔｏ－ＰＧＦ＿（１α）升高早于ＴＸＢ＿２，提示ＰＧＩ＿２参干旱期缺氧肺血管张力调节。（４）缺氧大鼠２周时肺动脉高压达到高峰，右心室明显肥厚，而肺组织ＴＸＢ＿２至缺氧４周后才见增加，表明ＴＸＢ＿２不是缺氧早期肺血管收缩的主要因素。     

实验性肾炎肾皮质TXA_2－PGI_2平衡失调与肾小球病理变化的关系

本文用阳离子化牛血清白蛋白制作大鼠原位性肾炎模型，观察血栓素Ａ＿２前列环素平衡的变化及与肾小球病理变化的关系。将模型动物随机分成２组，分别腹腔内注射Ｄａｚｏｘｉｂｅｎ、蒸馏水，共注射２周。结果显示，大鼠免疫２周后，肾皮质ＴＸＢ＿２升高，６－Ｋｅｔｏ－ＰＧＦ＿１α降低，尿蛋白量增加。４周后上述改变加重伴血小板聚集强度增大。治疗组大鼠肾皮质ＴＸＢ＿２降低，６－Ｋｅｔｏ－ＰＧＦ＿１α升高，ＴＸＢ＿２／６－Ｋｅｔｏ－ＰＧＦ＿１α比值降低，血小板聚集强度减弱，肾小球足突融合部分缓解，ＧＢＭ中电子致密物有溶解吸收迹象。统计处理提示，尿蛋白与ＴＸＢ＿２呈正相关（ｒ＝０．７８４４），与６－Ｋｅｔｏ－ＰＧＦ＿１α呈负相关（ｒ＝－０．７１６３）。表明原位性肾炎大鼠肾皮质存在着ＴＸＡ＿２－ＰＧＩ＿２平衡失调，肾小球病理变化与ＴＸＡ＿２－ＰＧＩ＿２平衡失调有关。     

急性低氧性肺动脉高压与磷脂酶A2活力关系初探

目的：探讨ＰＬＡ２及相关炎症介质在急性低氧性肺动脉高压形成中的作用。方法：用３０只ＳＤ大鼠随机分为三组（各１０只）：正常对照组（Ａ）、低氧组（Ｂ）、低氧加地塞米松组（Ｃ）。测定磷脂酶Ａ２活力（ＰＬＡ２）、血小板活化因子（ＰＡＦ）、前列腺素Ｅ２（ＰＧＥ２）、血栓素Ｂ２（ＴＸＢ２）。结果：Ｂ组低氧３０ｍｉｎ后，平均肺动脉压（ｍＰＡＰ）、血及肺中ＰＬＡ２活力、ＰＧＥ２、ＴＸＢ２、ＰＡＦ均明显增高；Ｃ组上述指标均明显低于Ｂ组。低氧情况下，ＰＬＡ２与ｍＰＡＰ、ＰＡＦ、ＰＧＥ２、ＴＸＢ２均呈正相关；ＰＡＦ、ＰＧＥ２、ＴＸＢ２分别又与ｍＰＡＰ呈正相关。结论：ＰＬＡ２通过相关炎症介质在急性低氧性肺动脉压的形成中可能起重要的介导作用。     

急性缺氧大鼠血浆、呼出气NO含量的变化及吸入NO对缺氧性肺血管收缩的影响

观察了大鼠急性缺氧前后血浆和呼出气一氧化氮（ＮＯ）含量的变化，结果显示，动物吸人１０％，２０ｍｉｎ后，血浆ＮＯ＿２／ＮＯ＿３浓度从２３．５６±７．１３升至４１．６３±１０．１０μｍｏｌ／Ｌ（Ｐ＜０．０１）；呼出气ＮＯ浓度出０．０９９±０．０５５增至０．１６２±０．１０８ｐｐｍ（Ｐ＜０．０１）．提示急性缺氧时ＮＯ生成增多可能在缺氮性肺血管收缩（ＨＰＶ）中起调节作用。为探讨吸入ＮＯ对ＨＰＶ的影响，本文采用人工呼吸给缺氧大鼠吸入４０ｐｐｍＮＯ，发现动物缺氧（１０％Ｏ＿２）１０ｍｉｎ后，平均肺动脉压（ｍＰＡＰ）和肺血管阻力（ＰＶＲ）较基础值明显升高（Ｐ＜０．０１）：而缺氧同时吸入４０ｐｐｍＮＯ１０ｍｉｎ，ｍＰＡＰ和ＰＶＲ较缺氧时明显降低（Ｐ＜０．０１），与基础值无显著差别（Ｐ＞０．０５），且发现△ＰＶＲ％为２．９４±９．８５％，较缺氧时６６．１８±２３．３９％明显降低（Ｐ＜０．０１），但吸入ＮＯ对体动脉压、体血管阻力，心输出量、血气和高铁血红蛋白无明显影响。从而提示吸入ＮＯ选择性降低缺氧性肺动脉高压且完全逆转ＨＰＶ。     

常压缺氧大鼠血浆和肺组织TXB2和6—keto—PGF1α的动态变化

本文观察常压缺氧２４ｈ及１，２，４ｗ后大鼠血小板数及聚集率和血浆及肺ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α的动态变化。结果表明（１）缺氧大鼠血小板数呈先增加、后恢复、再下降，血小板聚集率呈先减少、后增加再减少的动态变化。（２）血浆ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α均明显升高。（３）肺组织６－ｋｅｔｏ－ＰＧＦ１α升高早于ＴＸＢ２，提示ＰＧＩ２参于早期缺氧肺血管张力调节。（４）缺氧大鼠２周时肺动脉高压达到     

去除尺骨后桡骨的适应性骨再造

去除尺骨后桡骨的适应性骨再造＊董心朱兴华杨秀勤（吉林工业大学，长春１３００２５）ＡＤＡＰＴＡＴＩＯＮＡＬＢＯＮＥＲＥＭＯＤＥＬＩＮＧＯＮＴＨＥＲＡＤＩＵＳＡＦＴＥＲＴＨＥＵＬＮＡＲＯＳＴＥＯＴＯＭＹＤｏｎｇＸｉｎ，ＺｈｕＸｉｎｇｈｕａ，ＹａｎｇＸｉｕ...     

香烟烟雾抽提物对肺动脉内皮细胞环氧合酶，血栓素合成酶mRNA水平及PGI_2，TXA_2生成的影响

本实验应用放免测定及分子杂交技术观察了香烟烟雾抽提物（ＣＳＥ）对培养的猪肺动脉内皮细胞环氧合酶，血栓素合成酶基因表达和ＰＧＩ＿２，ＴＸＡ＿２生成的影响，进一步从分子水平探讨由内皮细胞产生的前列腺素在ＣＳＥ影响肺血管张力和ＨＰＶ中的作用。结果发现：在常氧或缺氧下，ＣＳＥ可促使内皮细胞环氧合酶—１ｍＲＮＡ水平升高于对照组的１．５倍，而环氧合酶—２ｍＲＮＡ则分别比对照组高２倍和１倍。同时在常氧或缺氧时，ＣＳＥ使内皮细胞条件培养基中６—ｋｅｔｏ—ｐＧＦｌａ．明显高于对照组（Ｐ＜０．０５）。然而，不论常氧或缺氧时，ＣＳＥ不影响血栓素合成酶基因表达和ＴＸＡ２的生成。提示在常氧和缺氧时，ＣＳＥ所致的环氧合酶ｍＲＮＡ水平升高及ＰＧＩ２增加介导了猪吸烟时肺血管张力和ＨＰＶ的降低。     

ADL DIFFCULTIES WITHIN THE HOME FOR A TETRAPLEGIC PATIENT

ＡＤＬＤＩＦＦＣＵＬＴＩＥＳＷＩＴＨＩＮＴＨＥＨＯＭＥＦＯＲＡＴＥＴＲＡＰＬＥＧＩＣＰＡＴＩＥＮＴＡＤＬＤＩＦＦＣＵＬＴＩＥＳＷＩＴＨＩＮＴＨＥＨＯＭＥＦＯＲＡＴＥＴＲＡＰＬＥＧＩＣＰＡＴＩＥＮＴＳｈｉＪｉａｎ；ＨｕａｎｇＭｉｎｑｉ；ＭａＸｉａｏｑｉ...     

Th1/Th2 balance in infection

Cytokines produced by T helper (Th) cells are of critical importance for the outcome of many infectious diseases. Producing the right set of Cyokines in response to an infectious agent can be a matter of life or death. The Th1/Th2 dichotomy, although an oversimplification has proven useful in the analysis of immune responses to infections. In some infectious diseases, most notably leishmaniasis or infections with gastrointestinal helminths, one Th subset is indispensable for clearing the infection, whereas the opposite Th subset is detrimental. More frequently, both Th1 and Th2 responses are required at different time points to effectively eradicate an infectious agent. The granuloma responses to eitherMycobacterium tuberculosis orSchistosoma mansoni provide illustrative examples and are discussed in this review. There is accumulating evidence for frequent coexpression of Th1 and Th2 Cyokines during the in vivo immune response to infections. The mechanisms by which infectious agents modulate Th1/Th2 phenotype development are summarized here. Finally, we review here the current evidence for cytokine imbalances induced by infections as pathogenic or protective factors in autoimmunity and allergy.     

Th1/Th2 balance in infection

Cytokines produced by T helper (Th) cells are of critical importance for the outcome of many infectious diseases. Producing the “right” set of Cyokines in response to an infectious agent can be a matter of life or death. The Th1/Th2 dichotomy, although an oversimplification has proven useful in the analysis of immune responses to infections. In some infectious diseases, most notably leishmaniasis or infections with gastrointestinal helminths, one Th subset is indispensable for clearing the infection, whereas the opposite Th subset is detrimental. More frequently, both Th1 and Th2 responses are required at different time points to effectively eradicate an infectious agent. The granuloma responses to eitherMycobacterium tuberculosis orSchistosoma mansoni provide illustrative examples and are discussed in this review. There is accumulating evidence for frequent coexpression of Th1 and Th2 Cyokines during the in vivo immune response to infections. The mechanisms by which infectious agents modulate Th1/Th2 phenotype development are summarized here. Finally, we review here the current evidence for cytokine imbalances induced by infections as pathogenic or protective factors in autoimmunity and allergy.     

The Th1/Th2 balance in autoimmunity

The study of autoimmune disease in the context of T-helper type 1 (Th1) and T-helper type 2 (Th2) CD4⁺ T-cell responses demonstrates that the relative contribution of either T-cell type to the development of a particular autoimmune response can influence whether or not this response leads to clinical disease. Moreover, this influence can be quite different depending on whether the particular disease process is cell mediated or antibody mediated. Recent studies have demonstrated that the development of Th1 and Th2 responses may be significantly influenced by the costimulatory molecules recognized by responding CD4 T cells, and by other undefined factors in the genetic background. It has also been demonstrated that autoreactive Th2 CD4⁺ cells can regulate the activity of disease-causing Th1 CD4⁺ T cells in vivo. Control of autoimmune disease may thus be achieved by procedures that regulate the relative contribution of Th1/Th2 CD4 T cells to an autoimmune response.     

Modulating the Th1/Th2 balance in inflammatory arthritis

The balance between Th1 and Th2 cells regulates the choice between inflammatory and antibody-mediated immune responses. To an increasing extent this balance is thought to involve the participation of antigen-presenting cells, rather than the entirely autonomous activity of T cells and their cytokines. Here we survey current opinion concerning the working of this balance, and its condition in rheumatoid arthritis and the other inflammatory arthritides. The contrast between Lyme arthritis and reactive arthritis is particularly illuminating, since one is triggered by extracellular and the other by intracellular infection. We describe current approaches to the modulation of this balance. Guided by the principles that genetic polymorphism is likely to identify relevant genes, that any cytokine gene picked up by a virus must matter and that natural immunosuppressive activity at mucosal surfaces should be worth exploiting, we identify as particularly worthy of attention: (i) IL-10, (ii) inhibitors of IL-12 production, (iii) inhibitors of CD40 ligand expression and (iv) oral and nasal tolerance. Other protective T cell subsets are touched on, and the impact of oligonucleotide arrays mentioned.     

Th1/Th2 lymphocyte balance in patients with aplastic anemia

Activated T cell plays an important role in the pathogenesis of aplastic anemia (AA). CD4+ T cells are divided into Th1 cells producing hematopoietic inhibitory cytokines like interferon-gamma and Th2 cells producing interleukin-4. We investigated the Th1/Th2 cell ratio in the peripheral blood of AA patients treated with immunosuppressive therapy (IST). There were 10 patients who responded well to IST (responders) and 3 patients who were refractory to IST (non-responders). Th1 cells were lower in responders than in non-responders (16.2+/-2.4% vs. 28.8+/-5.5%, respectively, p<0.05), whereas Th2 cells did not differ. The Th1/Th2 ratio was also significantly lower in responders than in non-responders, being 13.2+/-1.5 and 40.4+/-5.1 (p<0.001), respectively. In three responders, the Th1/Th2 ratio was declined according to the hematological recovery (from 10.6 to 8.3, 16.3 to 10.9 and 11.8 to 9.5). Our results suggest that Th1 lymphocytes are more predominant in AA, and it may be very useful to monitor the Th1/Th2 ratio during IST.