胆源性感染性休克兔血栓素、前列环素与血小板聚集率的变化

动态观察胆总管急性完全性梗阻并感染、继发休克兔的血浆血栓素(TXA_2)和前列环素(PGI_2)的稳定代谢产物 TXB_2和6-keto-PGF_(1α)含量及血小板聚集率的变化。结果,血浆 TXB_2呈进行性升高,20h 后(休克时)呈下降趋势,血浆6-keto-PGF_(1α)6h 升高,随后回降;血小板聚集率呈进行性下降。提示血栓素和前列环素、血小板聚集率的变化在重症急性胆管炎、胆源性感染性休克发病过程中起重要病理生理作用,与病情和预后转归有重要联系。     

［5－（4－甲脒－苄基）－2，4－二氧代－咪唑烷－3－基］－乙酰基－L－天冬氨酰－L－缬氨酸的合成

根据由精氨酸－甘氨酸－天冬氨酸组成的肽能抑制血小板聚集的机制，设计并合成了［５－（４－甲脒－苄基）－２，４－二氧代－咪唑烷－３－基］－乙酰基－Ｌ－天冬氨酰－Ｌ－缬氨酸（９）。生物试验结果表明：（９）抑制血小板聚集作用最强，其活性以ＩＣ＿（５０）值相比，强于类似物。     

Prevalence and mechanism of streptokinase-induced platelet stimulation. Effect of acetylsalicylic acid.

It was recently shown that streptokinase may induce clot formation in vivo by immunoglobulin G mediated platelet stimulation. We evaluated the in vitro effect of streptokinase on platelet function in 103 subjects, of whom 52 were < or = 30 years and 51 were > or = 50 years old. Although streptokinase inhibited platelet aggregation in the majority of cases, in nine the threshold concentration of ADP required to induce irreversible aggregation decreased with streptokinase (1 million Units. l-1) by 30% or more. This observation was confirmed in five of the nine by repeated measurements indicating reproducible streptokinase-induced platelet stimulation. Among the five, two were < or = 30, and three were > or = 50 years old. In none of the five subjects did the radio allergo sorbent test detect type E immunoglobulins directed against streptokinase in the serum. In contrast, in four of the five subjects, streptokinase-induced platelet hyperaggregability was suppressed by addition of goat antibodies against human immunoglobulin G, or F(ab')2-fragments of such antibodies. Acetylsalicylic acid did not prevent streptokinase-induced platelet stimulation, but in three of five cases, led to an increase in the control threshold concentration for ADP, so that after the decrease induced by streptokinase the threshold concentration for ADP was in the same range as before acetylsalicylic acid and streptokinase administration. Thus, streptokinase led to an inhibition of platelet aggregation in the majority of subjects evaluated. In a minority of five out of 103, however, streptokinase reproducibly caused platelet stimulation, presumably mediated by immunoglobulin G.(ABSTRACT TRUNCATED AT 250 WORDS)     

吸入麻醉药对人血浆和血小板血栓素B2生成与血小板聚集的影响

目的：探讨吸入麻醉剂氟烷、安氟醚和异氟醚对人血浆血栓素Ｂ２（ＴＸＢ２），血小板ＴＸＢ２生成与血小板聚集的影响。方法：血浆ＴＸＢ２和血小板ＴＸＢ２的生成量用放免分析法测量，血小板聚集率用比浊法测量。结果：吸入１ＭＡＣ氟烷３０分钟后，血浆ＴＸＢ２浓度、二磷酸腺苷（ＡＤＰ）和肾上腺素（Ｅ）诱导的血小板ＴＸＢ２生成量与血小板聚集率显著下降，吸入１ＭＡＣ安氟醚３０分钟后，血浆ＴＸＢ２浓度和血小板ＴＸＢ２生成量与血小板聚集率亦显著下降，其降低的程度比氟烷轻。吸入１ＭＡＣ异氟醚对上述指标无明显影响。血小板ＴＸＢ２生成的减少与血小板聚集率的下降呈显著正相关。结论：氟烷显著抑制血小板聚集，安氟醚次之，异氟醚对血小板聚集无明显影响。其机制可能与氟烷和安氟醚通过抑制血小板上血栓素Ａ２受体的亲和力，降低ＡＤＰ和Ｅ诱导的血小板ＴＸＢ２的生成有关。     

33例精神分裂症患者氯丙嗪治疗前后血小板聚集功能

本文对精神分裂症患者用氯丙嗪治疗前后PAg(T)功能进行观察及BPRS评定,发现精分症患者PAg(T)功能明显高于对照组,用氯丙嗪治疗1个月后,BPRS评定分值下降,患者临床症状消除,而PAg(T)第一时相无变化,第二时相明显升高,说明氯丙嗪聚药物可促发血小板释放内源性致聚物质,同时也说明患者PAg(T)异常不仅仅是情绪应激所致,更重要的是血小板生理功能异常。     

α_2受体阻滞后肾上腺素诱导的心衰病人血小板的聚集功能

先前的研究表明血小板α_2受体变化表征交感神经突触前α_2受体的变化。为了解心衰病人血小板α_2受体功能状况,我们观察了10例Ⅲ、Ⅳ级心功能的心衰病人及10例配对正常人由肾上腺素诱导的血小板聚集率在α_2受体阻滞前后的变化。结果表明肾上腺素诱导的血小板聚集率在两组无显著性差异,但应用α_2阻滞剂Rauwolscine(0.25mg/L)后,0.25,0.5,1.0mg/L E诱导的心衰病人血小板聚集率显著低于对照组,提示血小板α_2受体在心衰时有数量的减少或(和)功能的降低,表征交感神经突触前NE释放的负反馈机制被抑制。     

INVOLVEMENT OF PHOSPHOPROTEIN PHOSPHATASE 1 IN COLLAGEN-PLATELET INTERACTION

The binding of type I collagen to its receptor initiates platelet aggregation, but the relationship of the receptor to other signal transduction components is not yet established. Correlation of platelet aggregation and anti-type I collagen receptor antibody immunoprecipitation of type I collagen treated [³²PO4]-labeled platelets showed that there are two phosphoproteins (M_r 53 kDa and 21 kDa) that coprecipitated with the 65 kDa platelet type I collagen receptor. In the present investigation, we have identified one of the phosphoproteins. A soluble component the 100,000×g supernatant fraction of 53 kDa protein is recognized by polyclonal anti-PP1 antibody. The activity of the precipitated phosphatase is inhibited by okadaic acid and inhibitor 1, suggesting that it is protein phosphatase 1 (PP 1). Phosphorylation decreases PP 1 activity as was found with [³²PO4]-phosphorylase b as the substrate. The immunocoprecipitation of the type-1 collagen receptor and PP 1 inot the result of cross reactivity of the anti-type I collagen receptor antibody with the PP I protein. These results indicate that the platelet type I collagen receptor, PP 1, and unidentified 21 kDa protein are in close association with the platelet type I collagen receptor upon the binding of type I collagen by the receptor. Copyright © 1996 Elsevier Science Ltd     

癌胚抗原相关细胞黏附分子源性多肽KM17对血小板活化作用的研究

目的 探讨癌胚抗原相关细胞黏附分子（CEACAM1）源性多肽KM17对血小板聚集、释放、黏附功能的影响。方法 采用血小板聚集仪观察多肽KM17对凝血酶、胶原、花生四烯酸（AA）、二磷酸腺苷（ADP）等激动剂诱导的血小板聚集的影响;流式细胞术观察多肽KM17对ADP激活血小板后P-选择素释放的影响;显微镜下观察多肽KM17对血小板静态黏附于胶原基质的影响。结果 多肽KM17能显著促进ADP诱导的血小板聚集且呈剂量依赖（P <0.05）,而对AA、胶原及凝血酶诱导的血小板聚集差异均无统计学意义（P>0.05）;此外,多肽KM17对ADP激活血小板后P-选择素释放及血小板静态黏附于胶原基质的差异也无统计学意义（P>0.05）。结论 多肽KM17可明显促进ADP诱导的血小板聚集,但对ADP活化血小板后P-选择素释放及血小板静态黏附于胶原基质未见明显作用。     

红细胞聚集增高与纤维蛋白原的关系及其对心绞痛患者发病的影响

目的 :探讨红细胞聚集改变与纤维蛋白原的关系及其对心绞痛发病的影响。方法 :测定 80例不稳定性心绞痛患者和 40例健康人的红细胞聚集指数 (光密度法 )、红细胞变形指数 (激光衍射法 )、血浆及全血粘度 (旋转式粘度计 )和纤维蛋白原 (双缩脲法 )。结果 :不稳定性心绞痛患者红细胞聚集指数和全血粘度 ( 4 0s- 1 )及纤维蛋白原浓度均高于对照组 (P均 <0 .0 1～ 0 .0 5 ) ,且红细胞聚集指数与纤维蛋白原呈直线正相关 ,与全血粘度 ( 4 0s- 1 )无相关性。结论 :纤维蛋白原含量增加是红细胞聚集增强的主要原因之一 ;红细胞聚集能力增强导致血液高粘滞 ,与心绞痛发作有关 ;选择 10s- 1 以下切变率测定低切全血粘度 ,利于观察全血粘度与红细胞聚集的关系