白介素-6、血管内皮生长因子、D-二聚体对CSDH的影响

目的探讨血肿局部炎症、假膜新血管生成、局部纤溶状况及其在CSDH发生、发展中的作用。进而探讨CSDH的发病机制，并为CSDH的治疗及预防复发提供理论依据。方法以78例CSDH患者作为病例组，20例健康人作为正常对照组。采用ELISA法测定患者血清及血肿液中VEGF及IL-6的含量。比较患者末梢静脉血及血肿液中四种因子的含量变化并与正常对照组比较。结果病例组血肿液FDP、d-dimer检测均为阳性，血液为阴性；正常对照组血液FDP、d-dimer检测均为阴性；病例组血清VEGF含量与正常对照组比较差异无统计学意义。血肿液中VEGF浓度高于血清中。病例组血清IL-6浓度与正常对照组差异无统计学意义，血肿液中IL-6浓度高于血清中。CSDH患者血肿液VEGF、IL-6水平没有相关性。结论CSDH患者血肿液局部纤溶亢进，局部VEGF分泌旺盛，新血管生成活跃，局部炎症活跃，可导致CSDH不断扩大而参与CSDH发病机制。抗炎治疗、抑制VEGF的生理作用、有选择的对病人施行促凝治疗，可成为部分CSDH病人保守治疗及预防复发的有效手段。     

离体不同时间血痕的肉眼和扫描电镜观察

对离体不同时间血痕进行肉眼和扫描电镜观察，获得了血痕形态结构变化的初步认识．结果随时间延长，血痕逐渐干燥、龟裂，电镜下纤维蛋白网消失，其超微结构变化观察有助于血痕经过时间的推断．     

Endoscopic sealing of infected bronchus stump fistulae with fibrin following lung resections

Summary Bronchus stump insufficiency following lung resection, with an average incidence of 4%, is a serious complication which carries a mortality of up to 90%. Operative transthoracic approaches have been largely unsatisfactory because of the high operative risk and rapidly spreading infection. In an experimental study on 18 pigs, endoscopic occlusion of infected bronchus stump fistulae was achieved with fibrin sealant (1 ml, 500 units/ml thrombin, 3500 units/ml aprotinin) applied via a flexible bronchoscope. During autopsy, all bronchus stump fistulae were found to have healed after the second postoperative week. Transitory local abscesses of the pleura could be prevented by high-dose systemic antibiotic therapy for 5 postoperative days but not by antibiotics added to the fibrin sealant. This endoscopic method has already been performed successfully in 3 clinical cases; additional sclerotherapy with (2–3 ml Ethoxysclerol applied around the fistula orifice was carried out before fibrin sealing to stimulate fibrosis. Endoscopic controls demonstrated fistula closure by granulation tissue after 2 weeks. This procedure could become the method of choice for infected postoperative fistulae of the bronchus stump and should be attempted in any case before operative approaches are considered.     

前列腺癌组织中细胞外基质的免疫组织化学研究

为探讨前列腺癌（ＰＣａ）细胞的转移机制，应用免疫组织化学ＡＢＣ法在良性前列腺增生（ＢＰＨ）及ＰＣａ组织中对基膜连接蛋白（ＬＮ），胶原Ⅳ型蛋白（ＣＯＬⅣ），纤维连接蛋白（ＦＮ）等细胞外基质（ＥＣＭ）蛋白的表达进行检测，结果ＢＰＨ组织中基底膜部位ＬＮ，ＣＯＬⅣ及ＦＮ的染色呈连续线状分布，ＰＣａ组组织基底膜部位ＬＮ，ＣＯＬⅣ及ＦＮ的阳性染色呈碎片状或断线状分布。ＣＯＬⅣ在ＢＰＨ与ＰＣａ组织中的强阳性率无显著性差异（Ｐ＞０．０５）。结果提示ＥＣＭ在ＰＣａ组织中基底膜部位的明显缺失（非连续线状分布）可能是肿瘤转移的重要因素。     

纤维组织粘合剂的实验研究

本文应用“冷沉淀”法制备纤维组织粘合剂。对纤维组织粘合剂中主要成份和含量进行了测定,并测定了主要理化性质,建立了动物实验模型,观察了实验兔对纤维粘合剂的反应。     

急性白血病血浆及脑脊液D-dimer测定的临床意义

目的 探讨D-dimer(DD)在中枢神经系统白血病及急性白血病诊断、治疗中的价值。方法 采用ELISA法检测54例急性白血病(AL)患者脑脊液(CSF)DD水平，并对其中伴中枢神经系统白血病(CNSL)22例进行动态观察，同时检测7例上呼吸道感染，9例贫血患者CSFDD水平作对照。结果 CNSL组明显高于非中枢神经系统白血病(NCNSL)组及对照组。22例CNSL患者鞘内注射化疗药后。20例达完全缓解(CR)，DD值明显下降。2例无效者，CSFDD维持于较高水平。1例缓解后再次复发者，CSFDD含量再次升高。1例患者在CSF常规、生化确诊CNSL之前，CSF D-dirner已有改变。CNSL组CSFDD含量与CSF压力、白细胞数、蛋白含量均无明显相关关系。结论 DD对CNSL早期诊断、疗效观察、预后估计很有价值。     

股骨多段闭合骨折病人术前凝血功能的变化

目的 探讨股骨多段闭合骨折病人术前凝血功能的变化。方法 选择创伤股骨多段闭合骨折后当天入院的病人20例,年龄19-45岁,ASA Ⅰ级,为试验组(Ⅰ组);选择健康成年人15人,年龄21-39岁,作为对照组(Ⅱ组);Ⅱ组于清晨空腹采上肢静脉血标本,Ⅰ组病人入院后于骨折的第2天、第6天(手术当天清晨)空腹采上肢静脉血样本,检测血栓弹力图(TEG)指标[R时间、K时间、α角、血栓最大幅度(MA)、血栓硬度(G)]、D-二聚体浓度(D-Di)、血小板计数(PLC)及血小板聚集率(PAgR)的变化。结果 Ⅱ组TEG指标、D-Di、PLC及PAgR均在正常范围。与Ⅱ组比较,Ⅰ组骨折后第2天,K时间缩短(P<0.05),α角、MA、G及D-Di增高(P<0.01);骨折后第6天,R时间缩短(P<0.05),α角、MA、G、D-Di、PLC及PagR增高(P<0.01)。与骨折后第2天比较,Ⅰ组骨折后第6天MA、G、PLT及PAgR增高(P<0.05或0.01)。结论 病人创伤骨折后凝血功能24 h内增强,随时间的延长至术日呈高凝状态,应加强术中管理,并采取相应措施预防术中静脉血栓的发生。     

祛瘀消斑胶囊治疗不稳定型心绞痛及对其血浆Fib、DD的影响

目的　观察祛瘀消斑胶囊治疗不稳定型心绞痛及对其血浆Fib和DD水平的影响。方法　对 4 0例不稳定型心绞痛患者随机分为常规西药加祛瘀消斑胶囊治疗组 (治疗组 )和常规西药治疗组 (对照组 ) ,治疗组与对照组各 2 0例。采用相应药物治疗 4周后 ,观察 2组患者的临床疗效、心电图改善及硝酸酯类药物的停减率 ,以及血浆Fib、DD水平变化 ,并进行比较分析。结果　治疗组可显著改善心绞痛症状 ,与对照组比较有显著性差异 (P <0 .0 5 ) ,2组患者心电图改善情况及硝酸酯类药物减停率无显著性差异 (P >0 .0 5 )。治疗组降低Fib、DD水平 ,与对照组比较有显著性差异 (P <0 .0 5 )。 2组均未出现明显不良反应。结论　祛瘀消斑胶囊可显著降低不稳定型心绞痛患者Fib、DD水平 ,联合西药治疗不稳定型心绞痛 ,疗效优于单用西药 ,且安全可靠。     

Influence of heparin on fibrinogen and D-dimer plasma levels in acute myocardial infarction treated with streptokinase

The purpose of this study was to investigate whether, to whatextent, and through which mechanisms intravenous heparin, administeredbefore and after streptokinase, affects the plasma levels ofD-dimer and fibrinogen in myocardial infarction. Data concerningmortality and incidence of coronary recanalization in patientsreceiving heparin and thrombolytic therapy after acute myocardialinfarction are controversial; furthermore, the mechanisms throughwhich heparin acts in combination with thrombolytic therapyare unclear. Thirty-eight patients with acute myocardial infarctiontreated with streptokinase were considered. Nineteen of themreceived, immediately before the beginning of thrombolytic treatment,a bolus of heparin (100 U. kg¹ intravenously) and, 2 h later,intravenous heparin in doses raising the partial thromboplastintime to 2-2.5 times the normal value (Group 1); the remaining19 did not receive anticoagulant treatment (Group 2). Multipledeterminations of plasma D-dimer and fibrinogen levels wereobtained in all patients before, and in the seven days followingthrombolytic treatment. Six hours after streptokinase, fibrinogendecreased from 304 ± 34 to 61 ± 34 mg. dt¹ inGroup 1 and from 312 ± 29 to 38 ±21 mg. dt¹ inGroup 2 (P<002 versus Group 1). The same difference betweengroups persisted at the 12th and at the 18th hour. D-dimer values,from 0-5 ± 01 \ig. dl¹ in Group 1 and 04 ±01 fig.dt¹ in Group 2, increased at the 1st hour to 37.2 ± 36.5fig. dt¹ and 52.2 ± 39.8 µg. dl¹, respectively.A peak value was reached in both groups at the 6th hour, whichwas followed by a slow decrease. A significant difference betweenthe two groups (P<0.05) was observed at the 1st, 2nd, 4thand 6th hour. An inverse correlation between maximal changesof fibrinogen and of D-dimer was found in both groups (r= 0.89,P<0.001 in Group 1; r=-0.81, P<0.001 in Group 2). The relationship between D-dimer and fibrinogen variations afterstreptokinase and changes induced by heparin, support the hypothesisthat the decrease of fibrinogen, following thrombolysis, isnot only the consequence of its direct degradation, but alsothe result of its transformation by streptokinase into fibrin,fibrin cross-linked (with facilitation of thrombogenic condition)and then into the stable catabolite, D-dimer. These data confirma thrombogenic effect of streptokinase therapy; this tendencycan be limited by prompt use of high doses of heparin.     

In vivo measurements of fibrin formation and degradation in nephrotic patients

Summary Intraglomerular fibrin deposition has been implicated as an important pathogenetic mechanism in patients with glomerular diseases and the nephrotic syndrome. To investigate fibrin formation and degradation in nephrosis, we measured fibrinopeptide A by radio-immunoassay and D-dimer by enzyme-linked immunosorbent assay in the plasma of 30 consecutive adult patients with the nephrotic syndrome; in 10 the serum creatinine was more than 2 mg/dl. Both fibrinopeptide A and D-dimer were abnormally elevated in the majority of nephrotics (P<0.001 vs. healthy controls), providing evidence of increased fibrin generation and lysis “in vivo.” A positive correlation was found between fibrinopeptide A and D-dimer (correlation coefficient 0.64,P<0.001), suggesting a close relationship between fibrin formation and degradation. Calcium heparin, administered to 12 nephrotics, caused a marked decrease in plasma fibrinopeptide A, due to a reduction of in vivo thrombin activity. As enhanced thrombin activity can favor fibrin deposition within the renal parenchyma, as well as vascular complications, it is reasonable to assume that an antithrombotic treatment aimed at controlling thrombin generation may ameliorate the natural history of nephrosis.