通脉注射液活血通脉试验的药理学研究

目的:提供通脉注射治疗用于缺血性心脑血管疾病的益气活血的药效学依据。方法:以NS和复方丹参注射液分别作为阴性和阳性对照进行大鼠、小鼠研究。结果:通脉注射液对ADP诱导的血小板聚集有明显抑制作用,并能减少血小板细胞的粘附性;能显著延长大鼠的出血时间和小鼠的凝血时间,但对凝血酶原时间无影响;对毛细血管通透性的增高有明显的抑制作用。结论:通脉注射液有活血通脉作用。     

芪丹通脉片对家兔血小板聚集的影响

目的 :观察芪丹通脉片对实验性家兔血小板聚集的影响。方法 :连续 7天灌胃给药后 ,采用Bom氏比浊法测量其血小板聚集率。结果 :实验结果表明 ,与对照组比较 ,芪丹通脉片明显降低二磷酸腺甘(ADP)和花生四烯酸 (AA)诱导的家兔血小板聚集率 (P <0 .0 5～ 0 .0 1) ,对胶原诱导的家兔血小板聚集率有降低趋势。结论 :芪丹通脉片具有抑制血小板聚集的作用。     

磷酸化ERK1/2对大鼠体外血小板聚集的可能作用

目的：观察两种激动剂诱导下，MEK1/2抑制剂PD098059对大鼠体外血小板聚集及磷酸化ERK1/2的影响。方法： 采用比浊法测定血小板最大聚集率，并观察最大聚集率发生时间，以及PD098059对血小板聚集的抑制率；采用Westernblot测定ERK1/2磷酸化表达。结果： 凝血酶和ADP均可诱导血小板聚集及 ERK1/2磷酸化的表达；PD098059ADP降低血小板最大聚集率及ERK1/2磷酸化表达；凝血酶与ADP诱导的血小板最大聚集率、最大聚集率发生时间及对PDO98059的反应均有差异。结论： ERK1/2为血小板聚集的信号转导途径之一；但在不同激活剂引起的血小板聚集中所起的作用不尽相同。     

柚皮素通过PI3K/Akt通路拮抗血小板聚集的体外研究

目的:探讨柚皮素拮抗二磷酸腺苷(ADP)诱导的血小板聚集的作用及机制。方法:采用血小板聚集仪观察不同浓度柚皮素对ADP诱导的大鼠血小板聚集的影响。采用荧光显微镜观察柚皮素对血小板在固化纤维蛋白原上扩展功能的影响。采用Western blot检测磷脂酰肌醇3-激酶(PI3K)表达及蛋白激酶B(Akt)磷酸化水平。结果:柚皮素能剂量依赖性地抑制ADP诱导的体外血小板聚集,其半数抑制浓度(IC_(50))值为(132.1±31.7)μmol/L。柚皮素灌胃给药,对ADP诱导的大鼠体内血小板聚集也有明显的抑制作用。柚皮素还能显著抑制血小板在固化纤维蛋白原上的扩展。Western blot结果显示,柚皮素能明显抑制ADP刺激的PI3K表达和Akt磷酸化同时,PI3K广谱抑制剂LY294002能增强柚皮素对Akt磷酸化的抑制作用。结论:柚皮素可能通过抑制血小板PI3K/Akt信号通路发挥抗血小板聚集的作用。     

抗血小板糖蛋白VI单克隆抗体的制备及其功能研究

目的:制备抗血小板糖蛋白VI(GPVI)单克隆抗体,观察其在体外抗血小板黏附和聚集功能。方法:采用基因重组技术体外表达血小板糖蛋白VI胞外区重组蛋白(rGPVI)。以rGPVI免疫小鼠,经细胞融合及筛选后制备抗GPVI单克隆抗体。采用血小板聚集实验观察该单抗对胶原、Convu lxin及ADP诱导的血小板聚集的影响;利用平行板流动小室技术研究在高剪切力条件下该单抗对血小板在胶原表面黏附的抑制效果。结果:正确构建了rGPVI表达载体pET-20b(+)-GPVI,rGPVI在原核细胞中有效表达。rGPVI能够被抗Penta-H is单抗和抗GPVI多抗识别。制备的抗GPVI单克隆抗体SZ118能够识别rGPVI,并与血小板有特异的结合能力。SZ118能明显抑制纤维状胶原和Convu lxin诱导的血小板聚集,呈抗体剂量依赖性;对ADP诱导的血小板聚集无明显影响。血小板黏附实验表明,SZ118能够明显阻断在高剪切力条件下血小板与纤维状胶原表面的黏附。结论:成功制备抗GPVI单克隆抗体SZ118,该抗体与血小板有良好的结合能力,显著抑制胶原诱导的血小板聚集并明显降低血小板与胶原的黏附反应。     

抗血小板糖蛋白Ⅵ单克隆抗体的制备及其功能研究

目的：制备抗血小板糖蛋白Ⅵ（GPⅥ）单克隆抗体，观察其在体外抗血小板黏附和聚集功能。方法：采用基因重组技术体外表达血小板糖蛋白Ⅵ胞外区重组蛋白（rGPⅥ）。以rGPⅥ免疫小鼠，经细胞融合及筛选后制备抗GPⅥ单克隆抗体。采用血小板聚集实验观察该单抗对胶原、Convulxin及ADP诱导的血小板聚集的影响；利用平行板流动小室技术研究在高剪切力条件下该单抗对血小板在胶原表面黏附的抑制效果。结果：正确构建了rGPⅥ表达载体pET-20b（＋）-GPⅥ，rGPⅥ在原核细胞中有效表达。rGPⅥ能够被抗Penta-His单抗和抗GPⅥ多抗识别。制备的抗GPⅥ单克隆抗体SZ118能够识别rGPⅥ，并与血小板有特异的结合能力。SZ118能明显抑制纤维状胶原和Convulxin诱导的血小板聚集，呈抗体剂量依赖性；对ADP诱导的血小板聚集无明显影响。血小板黏附实验表明，SZ118能够明显阻断在高剪切力条件下血小板与纤维状胶原表面的黏附。结论：成功制备抗GPⅥ单克隆抗体SZ118，该抗体与血小板有良好的结合能力，显著抑制胶原诱导的血小板聚集并明显降低血小板与胶原的黏附反应。     

人参总皂甙对血小板聚集和环核苷酸代谢的影响

为了探讨人参总皂甙(Gensenosides GS)对血小板的作用及其机理,本文观察了GS对兔血小板聚集和环核苷酸代谢的影响。结果表明,GS(12mg/kg)由兔耳缘静脉给药后,曲花生四烯酸,ADP及胶胶诱导的血小板聚集率比给药前明显降低,同时测得血小板中cAMP含量比给药前明显升高,两个指标的时效曲线均大致呈双峰型,高     

两种血小板聚集分析仪检测结果的分析比较

目的 通过PL-11血小板分析仪(结果用最大聚集率,maximum aggregation rate,PL-MAR％表示)与光比浊法血小板聚集仪(light transmittance aggregometry,LTA,结果用血小板最大聚集率,LTA-MAR％表示)检测结果的比较分析,探讨两种方法的优略.方法 利用二磷酸腺苷(adenosine phosphate,ADP)诱导LTA的血小板聚集实验,ADP诱导PL-11血小板分析仪的血小板聚集实验.结果 ①对照组与患者组对比,LTA-MAR％,PL-MAR％参数有统计学差异(P＜0.01);②PL-MAR％与LTA-MAR％呈正相关(r=0.889).结论 ①氯吡格雷有抗血小板聚集的药物效果.②PL-11作为一种新型的血小板分析仪,检测结果与LTA检测结果相关性好,精密度高,可作为血小板聚集功能检测的新途径.     

白黎芦醇对高脂血症大鼠血脂、血小板聚集、释放功能的影响

目的:观察白藜芦醇对高脂血症模型大鼠血脂、血小板聚集、释放功能的影响.方法:高脂饲料复制高脂血症大鼠模型,全自动生化分析仪测定大鼠血浆TG,TC、LDLC,HDL-C水平,比浊法测定ADP诱导的血小板聚集率、双抗夹心放免法测定血浆GMP-140含量.结果:白藜芦醇大、中、小剂量组均能降低高脂血症大鼠血浆TG,TC、LDL-C水平,ADP诱导血小板最大聚集率及血浆GMP-140含量.结论:白藜芦醇对高脂血症大鼠具有降低血脂、抑制血小板聚集或释放的作用.     

天麻提取物对血小板聚集的影响

目的观察天麻提取物对家兔体外、大鼠半离体和小鼠体内血小板聚集的影响.方法用比浊法测定血小板的聚集率.结果在体外、半离体和体内实验中,天麻提取物G2能抑制由二磷酸腺苷（ADP）诱导的血小板聚集;在体外实验中,天麻提取物G2还能抑制由血小板活化因子（PAF）诱导的血小板聚集.结论天麻提取物G2具有显著的抗血小板聚集作用.     

血栓通注射液对LPS诱导的兔弥散性血管内凝血的拮抗作用

 目的：研究血栓通注射液对脂多糖（LPS）诱导的兔弥散性血管内凝血（DIC）的影响。方法：对兔耳缘静脉持续滴注LPS以建立兔DIC模型,记录各组动物在24 h后的生存率;全自动血浆分析仪测定丙氨酸氨基转移酶(ALT)和血尿素氮(BUN);用全自动凝血分析仪检测活化部分凝血活酶时间（APTT）和凝血酶原时间（PT）;用凝固法测定纤维蛋白原含量;全自动血细胞分析仪进行血小板计数;发色底物法测定蛋白C和抗凝血酶Ⅲ的活性;ELISA法检测血浆中肿瘤坏死因子α（TNF-α）的含量。结果：持续从兔耳缘静脉滴注LPS后,DIC模型组动物大量死亡,ALT和BUN显著升高,APTT和PT显著延长,蛋白C和抗凝血酶Ⅲ的活性明显降低,血小板计数明显减少,血浆中TNF-α的含量显著升高。注射血栓通注射液后,动物的死亡率明显下降,ALT和BUN明显下降,APTT和PT明显缩短,血小板计数明显上升,纤维蛋白原含量显著提高,蛋白C和抗凝血酶Ⅲ活性明显提升;血浆TNF-α的含量明显降低。结论：血栓通注射液对LPS所诱导的兔DIC有良好的拮抗作用。     

清开灵注射液对LPS诱导的兔弥散性血管内凝血的作用

目的: 研究清开灵注射液对脂多糖(LPS)诱导的兔弥散性血管内凝血(DIC)的作用。方法: 采用耳缘静脉持续滴注LPS的方法建立兔弥散性血管内凝血模型,观察各组动物24 h内各时点生存率;采用全自动凝血分析仪检测活化部分凝血活酶时间(APTT)和凝血酶原时间(PT);凝固法测定纤维蛋白原含量;全自动血细胞分析仪进行血小板计数;全自动血浆分析仪测定丙氨酸氨基转移酶(ALT)以及血尿素氮(BUN);发色底物法测定蛋白C及抗凝血酶Ⅲ的活性;ELISA法检测血浆肿瘤坏死因子α(TNF-α)含量。结果: 兔静脉持续滴注LPS后,APTT和PT显著延长,ALT和BUN显著升高,蛋白C和抗凝血酶Ⅲ的活性明显降低,血小板计数显著减少,血浆TNF-α含量显著升高。给予清开灵注射液后,APTT和PT的延长明显缩短,血小板计数、纤维蛋白原含量、蛋白C及抗凝血酶Ⅲ活性均明显恢复;ALT、BUN以及血浆TNF-α含量明显降低。结论: 清开灵注射液对LPS所诱导的兔弥散性血管内凝血有良好的拮抗作用。     

刺五加注射液(精制)治疗高粘血症的疗效观察

高粘血症不是一种独立的疾病,是许多疾病共同的病理基础,血粘度的增高往往是疾病的结果,又是一个致病因素,在疾病的发展过程中起促进作用,两者互为因果。刺五加注射液(精制)是由五加科植物刺五加的茎叶提炼而出,主要成分为含有总黄酮、异嗪皮定、丁香甙、刺五加甙等,主要通过降低血液粘稠度,降低血小板凝集功能使红细胞凝集性降低,降低红细胞压积,扩张脑血管,使缺血区血流量增加。本组观察刺五加注射液治疗后血液流变学有显著性改善,而对照组改善不明显。     

红花注射液对脂多糖诱导的兔弥散性血管内凝血的作用

 目的：研究红花注射液对脂多糖（LPS）诱导的兔弥散性血管内凝血（DIC）的作用。方法：兔耳缘静脉持续滴注LPS建立兔DIC模型。采用全自动凝血分析仪检测活化部分凝血活酶时间（APTT）和凝血酶原时间（PT）;凝固法测定纤维蛋白原含量;全自动血细胞分析仪进行血小板计数;发色底物法测定蛋白C及抗凝血酶Ⅲ的活性;全自动血浆分析仪测定丙氨酸氨基转移酶（ALT）和血尿素氮（BUN）;ELISA法检测血浆纤维蛋白（原）降解产物（FDP）和肿瘤坏死因子 α（TNF-α）含量。结果：DIC模型组APTT和PT进行性延长,ALT活性和BUN含量显著升高,蛋白C和抗凝血酶Ⅲ的活性显著降低,血小板计数进行性减少,血浆FDP和TNF-α含量显著升高。给予红花注射液后,DIC模型兔APTT和PT的延长明显缩短,血小板计数、纤维蛋白原含量、蛋白C及抗凝血酶Ⅲ活性均明显恢复,血浆ALT、BUN、FDP和TNF-α水平均明显降低。结论: 红花注射液对LPS诱导的兔DIC有较好的拮抗作用。     

复方丹参注射液抗脂多糖诱导的兔弥漫性血管内凝血

目的: 研究复方丹参注射液对脂多糖(LPS)诱导的兔弥漫性血管内凝血(DIC)的作用。方法: 用LPS诱导兔DIC模型。凝固法测定纤维蛋白原含量,全自动凝血分析仪检测活化部分凝血活酶时间(APTT)、凝血酶原时间(PT)和纤维蛋白原含量;全自动血细胞分析仪进行血小板计数;全自动血浆分析仪测定谷丙转氨酶(ALT)以及血尿素氮(BUN);发色底物法测定蛋白C及抗凝血酶Ⅲ的活性。观察复方丹参注射液对LPS诱导的兔DIC的拮抗作用。结果: 兔耳缘静脉持续滴注LPS,观察到:APTT和PT显著延长;血小板计数和纤维蛋白原含量明显减少;ALT和BUN显著升高;蛋白C和抗凝血酶Ⅲ的活性明显降低。给予复方丹参注射液后,APTT和PT的延长明显缩短;血小板计数和纤维蛋白原的含量均明显恢复;ALT和BUN显著下降;蛋白C及抗凝血酶Ⅲ的活性显著改善。结论: 复方丹参注射液对LPS诱导的兔DIC有良好的拮抗作用。     

杏丁注射液对糖尿病肾病患者血清活性氧水平及血液流变学指标的影响

目的:观察杏丁注射液对糖尿病肾病(DN)患者血清活性氧水平及血液流变学指标的影响。方法:将DN患者按自愿原则分为杏丁注射液治疗组和对照组。观察两组治疗前后血清超氧化物歧化酶(SOD)、谷光甘肽过氧化酶(GSH-Px)、丙二醛(MDA)及血液流变学指标的变化。结果:治疗前两组SOD、GSH-Px、MDA和血液流变学指标无明显差异。杏丁注射液治疗后SOD、GSH-Px较对照组明显升高,MDA明显降低(P<0.01);尿蛋白定量较对照组明显下降(P<0.01);低切全血粘度、红细胞压积、红细胞聚集指数和血小板聚集率较对照组和同组治疗前显著下降(P<0.01),而高切全血粘度和血浆粘度下降不明显;红细胞变形性显著增高(P<0.01)。结论:糖尿病肾病患者细胞抗氧化能力明显降低;杏丁注射液通过升高SOD、GSH-Px活性减缓肾组织细胞过氧化,从而达到迟发性肾小球硬化症的效果,改善血液流变性,对肾脏起保护作用。     

人体可供肌肉与静脉注射部位的探讨

肌肉与静脉注射是临床治疗的主要给药途径,也是护理工作的主要内容之一,但是,目前护理人员掌握的注射部位普遍比较单一,使注射工作受到一定限制。因而,如何使护理人员普遍能掌握更多的注射途径,仍是护理工作一个有价值的课题。笔者通过解剖学观察,认为人体有10处可供肌肉注射部位,16处可供静脉注射(以上包括目前常用的部位),为护理注射工作开辟了新的思路。     

Foamy cells in itp spleens and in granulomas induced by murine platelets, commercialized phospholipids, and erythrocyte membrane. Histological and ultrastructural studies

A large number of foamy cells were noted in the spleens from fourteen ITP patients, and two patients who received a large amount of platelet rich plasma. Using the unlabelled immunoperoxidase method, these foamy cells were shown to contain platelet antigen. Platelets in varying stages of intracellular digestion, from intact-appearing forms to myelin-like materials, were disclosed in foamy cells. Foamy cells were experimentally induced in granulomas by subcutaneous injection of platelets with or without accompanied administration of steroid, the platelets reacted with anti-murine platelet antibody, commercialized phospholipids (PE, PC, SM, PS, and the mixture of them), and the red blood cell membrane. The foamy cells induced by the subcutaneous injection of platelets are similar to those in the spleens of ITP patients. The lipid in foamy cells is chiefly derived from the membrane phospholipid of injected platelets. Concentric myelin-like materials were also noted in the foamy cells after injection of erythrocyte membrane. The myelin-like materials in these foamy cells are similar to those appearing in macrophages following injection of PC and SM. This suggests that these phospholipids derived from cell membrane are more resistant to intracellular digestion by lysosomal enzymes. We conclude that the foamy appearance of the cordal macrophage in ITP spleens results from incomplete intracellular degradation of platelet membrane.     

FOAMY CELLS IN ITP SPLEENS AND IN GRANULOMAS INDUCED BY MURINE PLATELETS, COMMERCIALIZED PHOSPHOLIPIDS, AND ERYTHROCYTE MEMBRANE

A large number of foamy cells were noted in the spleens from fourteen ITP patients, and two patients -who received a large amount of platelet rich plasma. Using the unlabelled immunoperoxidase method, these foamy cells were shown to contain platelet antigen. Platelets in varying stages of intracellular digestion, from intact-apperaring forms to myelin-like materials, were disclosed in foamy cells.
Foamy cells were experimentally induced in granulomas by subcutaneous injection of platelets with or without accompanied administration of steroid, the platelets reacted with anti-murine platelet antibody, commercialized phospholipids (PE, PC, SM, PS, and the mixture of them), and the red blood cell membrane. The foamy cells induced by the subcutaneous injection of platelets are similar to those in the spleens of ITP patients. The lipid in foamy cells is chiefly derived from the membrane phospholipid of injected platelets. Concentric myelin-like materials were also noted in the foamy cells after injection of erythrocyte membrane. The myelin-like materials in these foamy cells are similar to those appearing in macrophages following injection of PC and SM. This suggests that these phospholipids derived from cell membrane are more resistant to intracellular digestion by lysosomal enzymes. We conclude that the foamy appearance of the cordal macrophage in ITP spleens results from incomplete intracellular degradation of platelet membrane.     

Ultrastructural evidence for extravascular platelet recruitment in the lung upon intravenous injection of platelet-activating factor (PAF-acether) to guinea-pigs.

Bronchoconstriction and degenerative lesions of the bronchial epithelium were observed microscopically 1 min after the i.v. injection of 100 ng/kg of platelet-activating factor (PAF-acether) to the anaesthesized guinea-pig. Constricted arterioles containing marginated polymorphonuclear neutrophils and platelet aggregates were seen, as well as alveolar capillaries obstructed by thrombi formed by partially or totally degranulated platelets. Three minutes after the injection of PAF-acether, platelet diapedesis to the alveolar septa and lumen was clearly observed. Bronchoconstriction was still present at 3 min, but subsided after 60 min, whereas oedema of the submucosa persisted accompanied by an infiltration of eosinophils and neutrophils. The infusion of prostacyclin prevented the formation of platelet aggregates and platelet diapedesis due to PAF-acether, but the morphological evidence of bronchial constriction was not modified. Aspirin failed completely to modify the effects of PAF-acether. Our results show that PAF-acether causes early formation and deposition of platelet aggregates, accompanied by the margination of polymorphonuclear neutrophil leucocytes in pulmonary vessels of the guinea-pig. Since bronchoconstriction persisted when platelet aggregation was inhibited with prostacyclin, aggregation by itself would not account for this effect. Early platelet diapedesis in the vicinity of bronchial smooth muscle corroborates previous evidence that platelets contain and release bronchoconstrictor substances, which operate by cyclo-oxygenase-independent mechanisms and are possibly involved with the physiopathology of lung inflammation during immediate hypersensitivity.