六肽对兔血小板聚集活性的影响

目的研究六肽对兔血小板聚集活性的影响。方法采集健康家兔颈动脉血,以枸橼酸钠抗凝,用比浊法测其血小板在不同诱导剂诱导下聚集率。结果 1×10 5mol.L 1六肽,对兔ADP、花生四烯酸(AA)和凝血酶诱导的血小板聚集的抑制率分别为(66.22±1.40)%,(67.94±2.32)%和(58.18±4.67)%。六肽抑制兔ADP、AA和凝血酶诱导的血小板聚集的IC50分别为3.24×10 6mol.L 1,1.32×10 6mol.L 1和7.24×10 6mol.L 1。结论六肽在体外具有抑制兔血小板聚集的作用。     

鬼针草总黄酮对体外血小板聚集的影响

目的 探讨鬼针草总黄酮对家兔血小板聚集的影响. 方法 以二磷酸腺苷(adenosine diphosphate,ADP)及凝血酶(thrombase,Thr)作诱导剂,体外给予不同浓度鬼针草总黄酮溶液,比浊法测定血小板聚集率,观察鬼针草总黄酮对血小板聚集的抑制作用及量效关系. 结果 高、中剂量鬼针草总黄酮可降低由ADP所诱导的血小板最大聚集率(P<0.01),血小板聚集抑制率可达45.82%和28.65%;高、中剂量鬼针草总黄酮可降低由Thr所诱导的血小板最大聚集率(P<0.01),血小板聚集抑制率分别达48.36%,33.82%,作用强度呈浓度依赖性. 结论 鬼针草总黄酮对体外由ADP和Thr所诱导的血小板聚集具有较强的抑制作用.     

5—HT增强家兔ADP介导的血小板聚集反应

AIM: To study the enhanced effects of 5-hydroxytryptamine (5-HT) on ADP-induced aggregation. METHODS: Platelet aggregation was quantified by the light transmission, the cytosolic-free calcium ([Ca2+]i) was measured by digital fluorescent microscopy, and inositol 1,4,5-triphosphate (IP3) was determined by receptor binding assay. RESULTS: In rabbit platelet-rich plasma (PRP), 5-HT 0.03-3 mumol.L-1 induced a decrease in light transmission (DLT) in a concentration-dependent manner with centralization of granules, as revealed by electron microscopy. The DLT was accompanied with neither platelet aggregation nor a release reaction. In single washed platelets loaded with Fura-2, 5-HT caused a concentration-dependent elevation of [Ca2+]i, and IP3 level was also transiently increased in washed platelets at 15 s after stimulation by 5-HT. Adenosine diphosphate (ADP) also caused DLT transiently in PRP before its own aggregation without a release reaction. Pretreatment of PRP or washed platelets with 5-HT, the DLT by ADP was reduced concentration-dependently and ADP-induced aggregation and [Ca2+]i mobilization were enhanced. CONCLUSION: The enhancement of ADP-induced aggregation was attributed to the superimposition of the calcium release from the storage sites and calcium influx induced by ADP over the calcium release from the storage sites by 5-HT.     

昆布多糖对家兔血小板聚集和释放的影响

目的 观察昆布多糖对家兔血小板聚集和释放的影响.方法 采用体内试验,比浊法观察昆布多糖对血小板活化因子(PAF)诱导的家兔血小板聚集作用的影响,双抗夹心放射免疫法测定血浆血小板颗粒膜蛋白(GMP-140)含量.结果 昆布多糖能抑制血小板活化因子诱导的家兔血小板聚集,与生理盐水组相比有显著差异(P＜0.05或P＜0.01),并能降低血小板颗粒膜蛋白含量(P＜0.01).结论 昆布多糖具有抗血小板活化因子诱导的血小板聚集作用,能抑制血小板的聚集和释放.     

氨丁苯酞对血小板聚集功能的影响

目的　观察氨丁苯酞 (GZ 0 2 ) ,丁苯酞 (NBP)的结构衍生物对血小板聚集功能的影响。方法　参照Tamura法 ,观察GZ 0 2对局部脑缺血大鼠血小板聚集率的影响 ,并用比蚀法测定了GZ 0 2体内和体外给药对AA、ADP和胶原诱导的血小板聚集率的影响。结果　GZ 0 2能明显降低局部脑缺血大鼠血小板聚集率的异常增高 ,体内体外条件下均能明显抑制AA诱导的血小板聚集。结论　实验证明GE 0 2具有抑制血小板聚集功能的作用     

氯吡格雷对二磷酸腺苷诱导的血小板聚集的影响

目的 :探讨氯吡格雷对血小板聚集率的影响。方法 :血小板聚集率增高病人 2 4例 ,男性 1 4例 ,女性 1 0例 ,年龄 (5 9±s 1 0 )a。给予氯吡格雷5 0mg ,po,qd×4wk。在服药后 8d,4wk后用光学法测定血小板聚集率 (ADP诱导法 ) ,Duke法测定出、凝血时间 ,凝血因子Ⅰ及血小板计数。结果 :高血小板聚集率的病人使用氯吡格雷后血小板聚集率明显下降 ,治疗后 8d,4wk分别下降 (3 1±2 5 ) % ,(3 2± 2 1 ) % ,(P <0 .0 1 )。但出、凝血时间 ,血小板计数及凝血因子Ⅰ含量在使用氯吡格雷后无明显变化。结论 :氯吡格雷可有效拮抗ADP诱导的血小板聚集作用     

穿心莲内酯对二磷酸腺苷诱导血小板聚集的拮抗作用

目的：观察不同浓度穿心莲内酯提取物(APN)、穿心莲内酯单体(穿琥宁)对二磷酸腺苷(ADP)诱导血小板聚集的拮抗作用。方法：不同浓度穿心莲内酯提取物、穿心莲内酯单体分别加入人富含血小板血浆(PRP)中，用多功能血小板聚集仪测定ADP诱导的血小板聚集作用。结果：APN对ADP诱导血小板聚集有剂量依赖性抑制作用。结论：穿心莲内酯具有对抗ADP诱发的血小板聚集作用。     

维拉帕米对糖尿病病人体外血小板聚集的影响

糖尿病Ⅱ型病人２０例（男性１０例，女性１０例，年龄５８±ｓ７ａ）在０．５μｍｏｌ／ＬＡＤＰ作为血小板致聚条件下加入０．２５－１．０μｍｏｌ／Ｌ维拉帕米，观察对体外血小板聚集的影响。结果表明糖尿病Ⅱ型病人在二相聚集比正常者显著增强，维拉帕米在０．２５－１．０μｍｏｌ／Ｌ浓度范围内均可部分减缓糖尿病Ⅱ型病人所增高的血小板聚集。     

槲皮素对氧自由基诱发血小板聚集性变化的影响

目的：观察氧自由基的血小板聚集性的改变以及探讨槲皮素抑制血小板聚集可能性的作用机制，方法：利用黄嘌呤／黄嘌呤氧化酶体系产生的氧自由基，分别按改良Ｂｏｎｒ’ｓ法和化学发光法测定了血小板聚集性和氧自由基，结果：氧自由基能够加强低浓度ＡＤＰ（１．６μｍｏｌ．Ｌ＾－１）诱导的血小板聚集，聚集率从２９％－３８％增至５９％－７０％，此加强作用可被槲皮素或氢化可的松所取消，同时，槲皮素（４μｍｏｌ．Ｌ＾－１）和     

Influence of fenflumizole on platelet aggregation in man

Summary The anti-aggregatory effect of fenflumizole, a new non-steroidal anti-inflammatory imidazole derivative is described in a study in 6 healthy male volunteers, mean age 33 years. Arachidonic acid (AA), ADP, collagen aggregation, coagulation and fibrinolysis parameters were examined before, during and after treatment with oral fenflumizole first 50 mg b.i.d. for 4.5 d and then 200 mg/d for 5 days. During treatment the threshold concentration for collagen aggregation demonstrated hypo-aggregability in all subjects. No significant change was noted in ADP aggregation. AA-induced aggregation showed an increased threshold concentration during and for 7 days after fenflumizole administration. No significant change was seen in bleeding time, fibrinolysis or coagulation parameters. No side effects were observed during or after treatment. It is concluded that fenflumizole is a potent inhibitor of platelet aggregation ex vivo.     

不同剂量阿司匹林对冠心病患者血小板聚集功能的影响

目的探讨不同剂量阿司匹林对冠心病患者血小板聚集功能（PAG）的抑制作用。方法 248例冠心病患者随机分为A组62例、B组62例、C组63例、D组61例,4组阿司匹林口服剂量分别为每天50mg、100mg、200mg、300mg,服药前及服药2周后测定PAG。结果用药前后相比,4组不同剂量阿司匹林（50,100,200,300mg）对PAG均有一定的抑制作用。B组对PAG的抑制作用与A组比较差异无统计学意义（P〉0.05）。C组、D组对PAG的抑制作用明显优于B组,差异有统计学意义（P〈0.05和P〈0.01）,但C组与D组比较,差异无统计学意义（P〉0.05）。结论阿司匹林每天200mg可能是一个较合理的治疗剂量。     

不同剂量阿司匹林对冠心病患者血小板聚集功能的影响

目的 探讨不同剂量阿司匹林对冠心病患者血小板聚集功能(PAG)的抑制作用.方法 248例冠心病患者随机分为A组62例、B组62例、C组63例、D组61例,4组阿司匹林口服剂量分别为每天50mg、100mg、200mg、300mg,服药前及服药2周后测定PAG.结果 用药前后相比,4组不同剂量阿司匹林(50,100,200,300mg)对PAG均有一定的抑制作用.B组对PAG的抑制作用与A组比较差异无统计学意义(P>0.05).C组、D组对PAG的抑制作用明显优于B组,差异有统计学意义(P<0.05和P<0.01),但C组与D组比较,差异无统计学意义(P>0 05).结论 阿司匹林每天200mg可能是一个较合理的治疗剂量.     

Influence of ethanol and serotonin on rat platelet aggregation

We demonstrated that ethanol (1.0, 2.0 and 4.0 g/kg p.o.) significantly decreased blood platelet aggregation in a dose-dependent manner. The chronic administration of ethanol (6 g/kg daily for 4 weeks) also altered the sensitivity of rat platelets to ADP (4 mumol/l). We found that the acute and chronic administration of alcohol significantly increased the amplifying effect of 5-hydroxytryptamine (5-HT; 10(-6) mol/l) on ADP-induced aggregation. In all groups of rats, ketanserin (10(-5) mol/l) completely inhibited the amplification of aggregation induced by serotonin. In conclusion, the present results show that ethanol did not only produce inhibition of ADP-induced platelet aggregation but also affected the potentiating action of 5-HT on this process.     

Influence of new 1,3,4-thiadiazines on platelet aggregation in vitro and ex vivo

The influence of new original 1,3,4-thiadiazines on the human platelet aggregation in vitro was studied. All substances inhibited the platelet aggregation induced by both ADP and arachidonic acid. 1,3,4-Thiadiazines L-19, H-30 and L-37 were the most effective inhibitors. Effect of the intravenous injection of L-19 in various doses on platelet aggregation and some parameters of plasmatic hemostasis were studied ex vivo.     

Effects of high flavanol dark chocolate on cardiovascular function and platelet aggregation

Regular consumption of chocolate and cocoa products has been linked to reduced cardiovascular mortality. This study compared the effects of high flavanol dark chocolate (HFDC; 1064 mg flavanols/day for 6 weeks) and low flavanol dark chocolate (LFDC; 88 mg flavanols/day for 6 weeks) on blood pressure, heart rate, vascular function and platelet aggregation in men with pre-hypertension or mild hypertension. Vascular function was assessed by pulse wave analysis using radial artery applanation tonometry in combination with inhaled salbutamol (0.4 mg) to assess changes due to endothelium-dependent vasodilatation. HFDC did not significantly reduce blood pressure compared to baseline or LFDC. Heart rate was increased by LFDC compared to baseline, but not by HFDC. Vascular responses to salbutamol tended to be greater after HFDC. Platelet aggregation induced by collagen or the thromboxane analogue U46619 was unchanged after LFDC or HFDC, whereas both chocolates reduced responses to ADP and the thrombin receptor activator peptide, SFLLRNamide (TRAP6), relative to baseline. Pre-incubation of platelets with theobromine also attenuated platelet aggregation induced by ADP or TRAP6. We conclude that consumption of HFDC confers modest improvements in cardiovascular function. Platelet aggregation is modulated by a flavanol-independent mechanism that is likely due to theobromine.     

Influence of vasodilators used in the therapy of heart failure on platelet aggregation.

Of the vasodilators used at present in the treatment of heart failure, only nitroprusside and phentolamine inhibit platelet aggregation at therapeutic dose levels. The other vasodilators studied, viz. nitroglycerin, isosorbide dinitrate, hydrallazine, dihydrallazine and prazosin, only inhibit platelet aggregation at relatively high concentrations, well above those reached in vivo. The exact nature of the platelet receptor, stimulation and blockade of which respectively initiate and inhibit aggregation, is not yet know, but it would appear to resemble the presynaptic alpha-receptors of other tissues.     

Effects of cefonicid on platelet aggregation

Beta-lactam antibiotics may interfere with platelet aggregation by inhibiting the binding of agonists of platelet aggregation, such as ADP and collagen, to specific receptor sites. The aim of this study was to evaluate in vitro the effects of cefonicid, a semi-synthetic cephalosporin, on platelet aggregation. Spontaneous platelet aggregation and platelet aggregation induced by ADP and collagen were assessed. Platelets from healthy subjects were incubated with cefonicid at final concentrations of 0.1 mg/ml, 1 mg/ml and 10 mg/ml (0.1 mg/ml is the concentration of cefonicid achieved in humans at therapeutic doses). When compared with saline, cefonicid at a concentration of 0.1 mg/ml had no effect on platelet aggregation, but at 1 mg/ml it inhibited ADP-induced aggregation and at 10 mg/ml it also inhibited aggregation induced by collagen. These findings suggest that therapeutic doses of cefonicid do not affect platelet aggregation.     

雷公藤内酯醇诱导兔血小板聚集作用

雷公藤内酯醇 (Ｔｒｉｐｔｏｌｉｄｅ ,Ｔｒｉ)具有抗肿瘤、免疫抑制、抗炎等生物活性 ;临床上用于治疗银屑病 ,类风湿性关节炎及白血病[1] 。但在动物实验和临床应用中发现其静脉注射会引起严重的血栓性浅静脉炎 ;为探讨其引起血栓性浅静脉炎的机制 ,我们观察了Ｔｒｉ对兔血小板功能的影响。1　材料与方法1.1　材料　Ｔｒｉ由本所提取 ,纯度 99 9% ,使用时以 2 %丙二醇配成所需浓度。ＡＤＰ美国Ｓｉｇｍａ生产 ;5 ＨＴ瑞士Ｆｌｕ ｋａ生产 ;ＴＸＢ2 放免药盒 ,中国医学科学院基础所提供 ;ｃＡＭＰ和ｃＧＭＰ放免药盒 ,中国原子能研究所提…