甲状腺功能异常大鼠血浆心纳素和肾素相关性的探讨

实验比较了甲状腺功能亢进（甲亢）、甲状腺功能减退（甲减）和对照组大鼠血浆中心钠素（ＡＮＦ）、血管紧张素Ⅱ（ＡＴⅡ）和醛固酮（ＡＬＤ）的相关关系。结果表明甲亢大鼠血浆中ＡＴⅡ和ＡＬＤ明显高于对照组（Ｐ＜０．０５），而ＡＮＦ升高的更为明显（Ｐ＜０．０１）。相反甲减大鼠血浆ＡＬＤ明显低于对照组（Ｐ＜０．０５），而ＡＴⅡ和ＮＡＦ则降低的更为显著（Ｐ＜０．０１），结果提示在甲状腺功能异常的病理过程中，血浆Ａ     

飞龙掌血水提物对垂体后叶素所致大鼠缺血心肌的保护作用

目的：观察飞龙掌血水提物（Ｆ０１）对急性缺血心肌的保护作用。方法：采用垂体后叶素所致大鼠急性心肌缺血模型观察药物的作用。结果：Ｆ０１（１７５或３００ｍｇ／ｋｇ）及维拉帕米在大部分时点上能明显缓解垂体后叶素所引起的心电图Ｔ波变化（Ｐ＜００５或Ｐ＜００１）。垂体后叶素使对照组１００％的动物发生心律失常，而在Ｆ０１组（１００、１７５或３００ｍｇ／ｋｇ）及维拉帕米组中，心律失常的发生率分别为７０％（Ｐ＞００５）、４４％（Ｐ＜００５）、２０％（Ｐ＜００１）和１１％（Ｐ＜００１）。结论：Ｆ０１对垂体后叶素所致急性缺血心肌具有保护作用，其效应与剂量呈相关性。     

内毒素休克大鼠脑组织中氨基酸含量和钙含量的动态变化

目的：观察内毒素休克大鼠脑皮层中氨基酸含量和钙含量的动态变化。结果：对照组大鼠平均动脉压平稳（１６５±０．６）ｋＰａ；休克组平均动脉压明显下降，６ｈ死亡率９０％，伴随平均动脉压的变化，脑系数于６ｈ显著增大（Ｐ＜０．０５），脑皮层兴奋性氨基酸含量于１ｈ及３ｈ有显著升高（Ｐ＜０．０５），钙含量于６ｈ有显著升高（Ｐ＜０．０５）。结论：内毒素休克可引起脑兴奋性氨基酸含量的持续过度增加，由此而导致的脑功能改变可能在休克发展及转归中起重要的病理生理作用     

体外反搏治疗失血性休克中一氧化氮合酶的变化

目的：探讨反搏治疗失血休克中一氧化氮合酶（ＮＯＳ）的变化。方法：复制狗的失血休克模型，用同位素方法测定反搏前后各组织的ＮＯＳ活性。结果：体外反搏后平均动脉压较反搏前明显上升（Ｐ＜００１）。脑ＮＯＳ测定值假手术对照组明显高于失血休克组Ｐ＜００１）及失血休克克反搏组（Ｐ＜００１），失血休克组则明显低于失血休克反搏组（Ｐ＜００１）；心肌ＮＯＳ活性假手术对照组与失血休克反搏组均明显高于失血休克组（Ｐ＜００５，Ｐ＜００１），但假手术对照组与失血休克反搏组之间无显著差异（Ｐ＞００５）；主动脉ＮＯＳ活性假手术对照组明显高于失血休克组（Ｐ＜００１）及失血休克反搏组（Ｐ＜００５），但失血休克组与失血休克反搏组间无明显差异（Ｐ＞００５）。结论：体外反搏可以增强小血管ＮＯＳ活性，ＮＯＳ活性的恢复则可能在反搏治疗中起重要作用     

白细胞介素—8对大鼠失血性休克血浆6—keto—PGF1α和TXB2含量的影响

目的和方法：本文观察重组人内皮细胞衍生的白细胞介素－８（ｒｈＥＤＩＬ－８）对大鼠晚期失血性休克血浆６－ｋｅｔｏ－ＰＧＦ１α和ＴＸＢ２含量的影响，并与平均动脉血压（ＭＡＢＰ）的变化作相关性分析。结果：晚期失血性休克血浆６－ｋｅｔｏ－ＰＧＦ１α含量明显降低（１０６７４±１２２６ｖｓ１５６８２±１１４２）ｎｇ／Ｌ，Ｐ＜００１，ＴＸＢ２含量明显升高（３１８３６±２６．５４ｖｓ１７４９１±２１５８）ｎｇ／Ｌ，Ｐ＜００１；给予ｒｈＥＤＩＬ－８（２５０μｇ／ｋｇ）后，血浆６－ｋｅｔｏ－ＰＧＦ１α含量明显升高（３６８４７±１５６８ｖｓ１０３７６±１３１８）ｎｇ／Ｌ，Ｐ＜００１，其血浆水平与ＭＡＢＰ变化呈明显正相关（ｒ＝０．７４６，Ｐ＜００１）；ｒｈＥＤＩＬ－８对血浆ＴＸＢ２含量却无明显影响。结论：ｒｈＥＤＩＬ－８抗晚期失血性休克作用与其促进血管内皮细胞产生和释放ＰＧＩ２有关     

抗疲劳1号对游泳大鼠血液、肌肉和脑中ATP含量及血乳酸含量的影响

目的：观察抗疲劳１号（ＡＦ－１）对游泳运动大鼠血液ＡＴＰ和乳酸，以及脑和肌肉组织中ＡＴＰ含量的影响。方法：用生物发光法测定６组不同游泳强度大鼠血液和组织中ＡＴＰ含量；血乳酸含量变化用乳酸自动分析仪监测。结果：给药组大鼠游泳１０ｍｉｎ，血中ＡＴＰ含量明显高于对照组；血中乳酸含量明显低于对照组（Ｐ＜００１）。在游泳力竭鼠中，给药组血ＡＴＰ含量也较对照组高；而血乳酸含量较对照组低（Ｐ＜００５，Ｐ＜００１）。给药大鼠中，游泳１０ｍｉｎ组肌肉ＡＴＰ含量明显高于对照组（Ｐ＜００１）；游泳力竭组仍可保持在对照组水平（游泳时间不同）。给药鼠游泳１０ｍｉｎ和力竭两组脑组织中ＡＴＰ含量与未给药动物无明显差异，但未游泳组明显高于对照组。未游泳给药鼠肌肉中ＡＴＰ含量也明显高于对照组（Ｐ＜００５，Ｐ＜００１）。结论：抗疲劳１号具有抗疲劳功用，可能通过增加组织ＡＴＰ的生成和贮存，促进能量代谢，减少乳酸堆积，进而增加运动强度及运动时间     

哮喘患者支气管肺泡灌洗液中细胞分类及其T细胞亚群的改变

目的和方法：采用间接免疫荧光法和支气管肺泡灌洗液（ｂｒｏｎｃｈｉａｌａｌｖｅｏｌａｒｌａｖａｇｅｆｌｕｉｄ，ＢＡＬＦ）技术观察１２例过敏性哮喘患者和２３例健康人外周血和ＢＡＬＦ中的Ｔ淋巴细胞亚群变化：结果：与健康对照组比较，过敏性哮喘患者外周血的Ｔ淋巴细胞亚群无明显改变，但其ＢＡＬＦ中的ＣＤ４＋细胞显著增高（５４．９７±４１４）％ｖｓ（７９．７１±９．６３）％，Ｐ＜００５；ＣＤ４＋与ＣＤ８＋细胞的比值也显著增高（１６４±０．３２ｖｓ２．３２±０．８３，Ｐ＜００５）。此外，过敏性哮喘患者ＢＡＬＦ中肥大细胞和嗜酸细胞百分比（００９±０．０４）％和（３６２±１．０６）％明显高于健康对照组（００２±０．０１）％和（０．３９±０．３０）％，Ｐ＜００５和Ｐ＜００１。结论：ＣＤ４＋细胞在哮喘的气道炎症中发挥重要作用。     

大鼠脑缺血及再灌流对脑组织血流量、ATP和乳酸水平含量的影响

目的和方法：本研究采用大鼠可逆性阻塞大脑中动脉所致的局灶性脑缺血再灌流模型，观察缺血３ｈ再灌流３ｈ、缺血６ｈ再灌流３ｈ对脑组织脑局部血流量（ｒｅｇｉｏｎａｌｃｅｒｅｂｒａｌｂｌｏｏｄｆｌｏｗ，ｒＣＢＦ）、ＡＴＰ、乳酸及脑水含量的影响。结果：缺血３ｈｒＣＢＦ明显下降（Ｐ＜００１），再灌流３ｈ升至缺血前６５３％（Ｐ＜００１）。缺血３ｈ再灌流３ｈ与缺血６ｈ组比较，ＡＴＰ明显恢复（Ｐ＜００１），乳酸含量明显下降（Ｐ＜００１），脑水含量明显减少（Ｐ＜００５）。缺血６ｈ再灌流３ｈ与缺血９ｈ组比较，尽管ＡＴＰ明显恢复（Ｐ＜００１），乳酸含量下降（Ｐ＜００１），但脑水含量无显著差异（Ｐ＞０１）。结论：缺血３ｈ再灌流３ｈ保护“半暗带”的效果优于缺血６ｈ再灌流３ｈ。     

α—MSH对内毒素性发热效应及下丘脑cAMP含量的影响

目的：观察α－黑素细胞刺激素（α－ＭＳＨ）对内毒素（ＥＴ）发热效应及下丘脑组织环一磷酸腺苷（ｃＡＭＰ）含量的影响。结果：α－ＭＳＨ能明显抑制ＥＴ引起的体温升高（Ｐ＜００５），同时降低ＥＴ引起的下丘脑组织ｃＡＭＰ含量的升高（Ｐ＜００１）；而对正常家兔体温及下丘脑组织ｃＡＭＰ含量均无影响（Ｐ＞００５）。结论：α－ＭＳＨ抑制中枢发热介质ｃＡＭＰ的生成可能是降低ＥＴ发热效应的主要机制之一。从而证明发热时中枢神经不但存在正调节途径，也存在负调节途径，体温上升的水平是正调节和负调节相互作用的结果     

二尖瓣狭窄和射频消融后患者血小板膜糖蛋白Ⅳ及凝血酶敏感蛋白的分布

目的：探讨二尖瓣狭窄患者及射频消融术后患者血小板功能状态。方法：运用流式细胞术测定阵发性室上性心动过速（ＰＳＶＴ）患者（ｎ＝１２）射频消融术（ＲＦＣＡ）前、后及二尖瓣狭窄（ＭＳ）患者（ｎ＝１４）股动脉血小板膜糖蛋白Ⅳ（ＧＰⅣ）及凝血酶敏感蛋白（ＴＳＰ）的分布。结果：ＭＳ患者及ＰＳＶＴ患者ＲＦＣＡ后静息血小板膜ＧＰⅣ分布明显多于ＰＳＶＴ患者ＲＦＣＡ前（Ｐ＜０．０５,＜０．０１）;ＭＳ患者静息血小板膜ＴＳＰ分布显著多于ＰＳＶＴ患者ＲＦＣＡ前（Ｐ＜０．０５）,而ＰＳＶＴ患者静息血小板膜ＴＳＰ分布ＲＦＣＡ前后无显著差异（Ｐ＞０．０５）;在凝血酶（０１Ｕ／ｍＬ,０．５Ｕ／ｍＬ）激活时,ＭＳ患者及ＰＳＶＴ患者ＲＦＣＡ后血小板膜ＧＰⅣ及ＴＳＰ分布均显著多于ＲＦＣＡ前（Ｐ＜０．０５,＜０．０１）。结论：ＭＳ患者及ＰＳＶＴ患者ＲＦＣＡ后血小板的活性及反应性增加,血小板发生不可逆聚集的危险性增高。     

粥样硬化斑块中组织因子和组织因子途径抑制物的表达

目的 观察股动脉粥样硬化斑块中组织因子TF和组织因子途径抑制物TFPI的表达、分布.方法 采用免疫组化、双染组化方法检测股动脉粥样硬化斑块中TF和TFPI的表达和分布,RT-PCR检测TF mRNA和TFPI mRNA的表达.脐动脉作为对照.结果 脐动脉外膜表达少量TF和TFPI蛋白及其mRNA,而动脉粥样硬化斑块血管增生内膜大量表达TF和TFPI蛋白及其mRNA.结论 增生内膜中所有细胞类型及细胞间质都表达TF和TFPI.     

Intra-articular tissue factor/factor VII complex induces chronic arthritis

OBJECTIVE: Fibrin accumulation in the joint cavity is a common feature of chronic arthritides, such as rheumatoid arthritis (RA). Complex formation between tissue factor (TF) and factor VII (FVII) is the initial step in such a fibrin formation. METHODS: To assess the role of the TF/FVII complex in the pathogenesis of joint inflammation, 1) the levels of TF/FVII complex were measured in synovial fluid of RA patients; 2) the complex was injected to healthy mice intra-articularly. RESULTS: Morphological analysis of the joints 4 days after TF/FVII injection revealed influx of CD4-Mac1+ mononuclear leukocytes into synovial tissue followed by cartilage and bone destruction. Inflammation induced by TF/FVII complex was more profound than that caused by each of the proteins separately, both with respect to frequency, severity and duration of arthritis. Interaction between macrophages and lymphocytes in sustaining joint inflammation was proved by the requirement of the combined lymphocyte/ monocyte depletion to abolish TF/FVII induced arthritis. Induction of monocyte attracting chemokines (MIP-1 alpha and RANTES) was shown to be one of the potential mechanisms for TF/FVII complex triggered inflammatory cell influx. Interestingly, TF/FVII complexes were detected in synovial fluid of 20/40 patients with RA. CONCLUSIONS: Altogether these findings indicate that TF/FVII complexes, frequently found intra-articularly in joints of RA patients, may be an important component in both induction and progression of chronic destructive arthritis.     

Plasma tissue factor levels and salivary tissue factor activities of periodontitis patients with and without cardiovascular disease

The association between periodontal and cardiovascular disease has received considerable attention. Studies have demonstrated a higher incidence of atherosclerotic complications in patients with periodontal disease. Tissue factor (TF) has been known as a key initiator of the coagulation cascade, and the TF pathway is the primary physiological mechanism of initiation of blood coagulation. Recently, it has been shown that the circulating pool of TF in blood is associated with increased blood thrombogenicity in patients with coronary artery disease (CAD). Various tissues and saliva have been known to have TF activity. Consequently, the aim of this study was to investigate plasma TF levels and TF activity of saliva in periodontitis patients with and without diagnosed CAD. Twenty-six patients with a diagnosis of CAD and 26 systemically healthy patients were examined in the dental clinic, and the Community Periodontal Index Treatment Needs (CPITN) scores were recorded. Plasma TF levels were determined using commercially available ELISA kit. Salivary TF activities were determined according to Quick's one-stage method. Plasma TF levels were significantly increased in patients with CAD when compared with the control group. There was no difference in salivary TF activities between the 2 groups, but there was a strong and negative correlation between salivary TF activities and CPITN indexes in both groups. In order to determine the possible role of TF activity as a salivary marker in CAD and periodontitis and to fully understand the negative correlation between salivary TF activities and CPITN, TF activity of gingival crevicular fluid that may also affect saliva can be evaluated.     

Connective tissue growth factor and cardiac fibrosis

Cardiac fibrosis is a major pathogenic factor in a variety of cardiovascular diseases and refers to an excessive deposition of extracellular matrix components in the heart, which leads to cardiac dysfunction and eventually overt heart failure. Evidence is accumulating for a crucial role of connective tissue growth factor (CTGF) in fibrotic processes in several tissues including the heart. CTGF orchestrates the actions of important local factors evoking cardiac fibrosis. The central role of CTGF as a matricellular protein modulating the fibrotic process in cardiac remodelling makes it a possible biomarker for cardiac fibrosis and a potential candidate for therapeutic intervention to mitigate fibrosis in the heart.     

一期凝固法测定尿液组织因子促凝活性的方法学建立

目的建立一种简便检测尿液组织因子促凝血活性的方法。方法以owren-koller稀释液5倍稀释尿液后,在STAGO全自动凝血仪检测凝固时间,通过兔脑粉不同浓度及其对应的凝固时间确定相应的标准曲线,计算出尿液组织因子（TF）的促凝血活性（TF-PCA）,并对该方法进行评价。结果通过owren-koller稀释液处理尿液有效解决了尿液理化因素变异大、干扰物质多等对TF活性检测的影响,TF中和单抗可有效抑制PCA活性,说明尿液PCA活性源于TF。TF-PCA测定方法学评价：总不精密度分别小于7%,表明该方法重复性尚可,平均回收率为80.8%,最低检测限为5mu/L,并在15～2200mu/L之间线性良好。结论一期凝固法是一种简便、结果可靠的检测尿液TF-PCA的方法。     

血小板相关组织因子的研究现状

血小板在生理性止血过程中居于中心地位,通过黏附、释放、聚集等反应来完成正常的止血过程,以助于维持血管壁的完整。血小板相关组织因子（TF）亦是血细胞源性TF的重要组成部分,TF与肿瘤、心血管疾病、糖尿病、炎症、血栓形成有关。并且不同的抗血小板药物对TF的表达有不同程度的影响。文章对最新发现的血小板相关TF在药物、凝血、心血管研究概况进行了综述,并推测了其可能在生理及病理情况下的重要意义。     

A multiplicative correction factor for tissue heterogeneities

A new multiplicative correction factor for tissue heterogeneities based on an exact expression for homogeneous non-unit-density media is proposed. O'Connor's density scaling theorem is invoked to evaluate the medium-specific tissue-maximum ratios used in the exact formulation. Monte Carlo calculations were performed at energies ranging from 60Co to 15 MV to test the technique for single- and multiple-slab geometries as well as for the clinical benchmark problem described recently by Orton et al consisting of a six-field lung plan. Within the level of statistical uncertainty (less than 2%) in the Monte Carlo calculations, the new correction factor agrees with the calculated data for single slabs of non-unit-density material. For the multiply layered geometries, the correction factor accurately represents the data beyond the build-up region at any interface, but is less reliable close to a boundary. For high energies, however, it is more accurate in the build-up region than other commonly used correction techniques such as the ratio-of-TMR or Batho methods. For all energies considered, the new correction factor agrees with the data measured by Orton et al to within 1.5%. It is more accurate than other correction factors considered by Orton et al at high energies, and is competitive with the Batho and equivalent TAR methods at low energies.