电阻法检测汇集血小板聚集功能试验的应用

血小板聚集功能是影响机体止血和血栓形成过程中的重要因素之一,血小板聚集率是反映血小板聚集功能的重要指标,目前检测血小板聚集率的方法很多,临床上常用比浊法,电阻法是一种较新型的检测血小板聚集率的方法 ,我们利用电阻法、用ADP和胶原分别作为血小板聚集诱导剂检测了汇集白膜层方法制备的去白汇集血小板的聚集率,报告如下。1材料与方法     

硝苯吡啶治疗脑血栓时血小板聚集功能变化

本文报道40例脑血栓患者,经口服硝吡苯啶药物治疗,有效率为87.5％,显效率为72.5％,其作用机制与硝苯吡啶能部分抑制缺血后细胞外钙离子进入细胞内,减少缺血性脑损伤有关。在用药前后采用两种诱导剂做了血小板聚集功能动态观察,治疗前血小板聚集性明显高于正常人(P<0.01)。提示:脑血栓患者血小板聚集性增高是形成血栓的关键。治疗后血小板聚集功能明显低于治疗前(P<0.01),说明硝苯吡啶具有降低血小板聚集功能,可能是钙离子拮抗剂抑制钙离子促发血小板聚集作用所致。     

异丙酚静脉麻醉对大面积烧伤患者血小板聚集及凝血功能的影响分析

目的分析对大面积烧伤患者使用异丙酚静脉麻醉后,血小板聚集和凝血功能受到的影响。方法将我院收治的40例大面积烧伤患者分为对照组和观察组,分别对其实施氯胺酮麻醉以及异丙酚麻醉,比较其血小板聚集和凝血功能情况。结果相比对照组,观察组的血小板聚集率、血小板钙离子以及凝血指数均明显更低,差异均有统计学意义(P<0.05)。结论在对大面积烧伤患者麻醉时,异丙酚可降低血小板钙离子和血小板聚集率,保证到凝血功能稳定性。     

地尔硫(艹/卓)联合东菱克栓酶治疗不稳定心绞痛

东菱克栓酶是一种新型单成分溶血栓改善微循环治疗剂,地尔硫[艹卓]作为新一代钙离子拮抗剂,能直接扩张冠脉,抑制血小板聚集,解除冠脉痉挛。     

血小板聚集性与冠状动脉支架术后支架内再狭窄的关系

<正>经皮冠状动脉介入治疗(PCI)是目前治疗冠心病安全有效的方法之一,但PCI术后血管再狭窄发生率为10%~15%[1]。P选择素(CD62p)位于血小板颗粒膜上,是反映血小板活化程度和血管内皮损伤的分子标志物。血小板聚集率是反映血小板聚集功能的一个重要指标[2]。本研究主要通过观察冠心病患者PCI术前后P选择素和血小板聚集率变化的情况,研究支架内再狭窄与血小板聚集性之间的关系,为更好了解PCI术后血管支架术后再狭     

高血压病患者血小板胞浆游离钙与血小板聚集功能的关系

高血压病患者血小板胞浆游离钙与血小板聚集功能的关系山西医科大学第二医院（０３０００１）丁康王凤芝山西省政府卫生所孙艾萍血管平滑肌细胞内胞浆钙离子（Ｃａ２＋）浓度决定血管的紧张程度，且是血管收缩的触动剂，因此，Ｃａ２＋在高血压病的发生和发展中起重要作用...     

尖吻蝮蛇毒小分子多肽的分离及抗血小板聚集作用

目的从尖吻蝮蛇毒中分离纯化一种抗血小板聚集小分子多肽,研究其理化性质以及对ADP、胶原、凝血酶诱导的血小板聚集反应的影响。方法经SephadexG-75凝胶过滤,超滤,DEAE-SepharoseCL-6B离子交换层析法分离纯化蛇毒组分,采用高效液相鉴定纯度,用SDS-凝胶电泳(SDS-PAGE)测定其分子量,用比浊法测定其抗血小板聚集活性。结果从尖吻蝮蛇毒中分离相对分子质量约为7862u等电点为4.29的组分,该组分能抑制由ADP、胶原、凝血酶诱导的血小板聚集并成剂量依赖性。结论此法成功地从尖吻蝮蛇毒中纯化出抗血小板聚集组分。该组分与去整合素比较相似,可能属于去整合素家族。     

维拉帕米对冠心病病人血小板功能状况的影响

冠心病病人血小板功能活性增高,钙离子对血小板的激活起重要作用,特别是细胞内钙离子和循环的核苷酸共同参与血小板的激活过程。血小板活性过高,导致血栓形成并发血液动力学障碍,在一定程度上决定着冠心病的经     

异搏定抑制血小板聚集的体外实验研究

异搏定——一种钙离子通道阻滞剂,在心血管内科作为常用药已有很久历史。近年来发现异搏定具有抑制血小板功能的作用,临床用途也越来越受到重视。我们在体外研究了异搏定对ADP诱导的血小板聚集功能的影响,观察低浓度和高浓度异搏定对血小板抑制作用。现报导如下。材料与方法本组20例为门诊和住院病人,其中脑血管病7例,癫痫3例,偏头痛2例,精神病     

槲皮素对血小板聚集和胞浆游离钙的影响(英文)

目的:研究槲皮素对凝血酶诱导的血小板聚集和胞浆游离钙浓度的影响及钙对槲皮素的血小板聚集抑制效应的作用。方法:用荧光钙离子指示剂观察槲皮素对血小板胞浆游离钙的影响.结果:槲皮素明显抑制凝血酶诱导的血小板聚集和游离钙的升高.IC_(50)和95％可信区间分别为146.2(92.4～231.3)和78.5(49.5—124.4)μmol·L~(-1).槲皮素对血小板的抑制作用可被钙翻转.槲皮素对凝血酶诱导的钙释放无影响.结论:抑制钙内流是槲皮素抑制血小板聚集和[Ca~(2 )]_i升高的机制.     

心肌钙反常模型细胞因子的表达及地尔硫卓的干预作用

目的探讨心肌钙反常模型诱导心肌细胞因子的表达及地尔硫卓的干预作用。方法采用Langendorff装置对离体大鼠心脏进行钙反常灌流(无钙灌流液5min,立即换正常钙灌流液灌流30min),建立心肌细胞钙超载模型。设立钙超载组、正常对照组、无钙对照组、钙超载给药组(地尔硫卓)和无钙给药组。电镜和光镜观察心肌病理和超微结构的变化。原子分光光度计检测心肌钙离子浓度,RT-PCR法测心肌细胞因子TNF-α、IL-1β、IL-6、TGF-β1和IL-10的表达。结果钙超载组光镜下未见明显炎症细胞浸润,电镜结果显示心肌细胞膜、细胞核和线粒体明显破坏。与正常对照组比较,TNF-α、IL-1β和IL-6明显增高,而TGF-β1和IL-10无明显变化。钙超载给药组(地尔硫卓)显示心肌损伤明显改善,TNF-α、IL-1β和IL-6明显下降。正常对照组、无钙对照组和无钙给药组心肌光镜和电镜下无明显差异,心肌Ca2+浓度差异无统计学意义,细胞因子的表达差异也无统计学意义。结论心肌钙反常模型诱导心肌表达TNF-α、IL-1β和IL-6,对TGF-β1和IL-10无明显影响,地尔硫卓能抑制心肌细胞钙超载诱导的TNF-α、IL-1β和IL-6表达。     

Inhibition of aggregation of rabbit and human platelets induced by adrenaline and 5-hydroxytryptamine by KB-R7943, a Na(+)/Ca(2+) exchange inhibitor

1. We investigated the effect of KB-R7943, a Na(+)/Ca(2+) exchange inhibitor, on the aggregation response induced by adrenaline and 5-hydroxytryptamine (5-HT), alone or in combination in human and rabbit platelets in the presence or absence of ouabain. 2. KB-R7943 inhibited aggregation induced by the combination of adrenaline and 5-HT in a concentration-dependent manner. The IC(50) values of KB-R7943 were 4.2+/-2.0 or 3.0+/-0.7 microM with washed rabbit platelets with or without ouabain pretreatment, respectively. 3. In platelet-rich human plasma, the aggregation was biphasic. The IC(50) value of KB-R7943 was 17.2+/-4.4 microM for the first phase aggregation. 4. KB-R7943 did not inhibit the first phase of aggregation induced by adrenaline alone, or the monophasic aggregation induced by 5-HT alone. 5. The aggregation of rabbit platelets depended on the presence of K(+) in the medium, and K(+)-dependent and K(+)-independent Ca(2+) influx were observed in resting platelets. Ouabain treatment increased only the K(+)-dependent but not the K(+)-independent Ca(2+) influx. 6. KB-R7943 inhibited K(+)-dependent Ca(2+) influx with or without ouabain pretreatment, but not K(+)-independent Ca(2+) influx. 7. From these results, we conclude that KB-R7943 inhibits the adrenaline plus 5-HT induced aggregation of rabbit and human platelets by inhibiting K(+)-dependent Na(+)/Ca(2+) exchange (NCKX). Our results suggest that NCKX plays an important role in platelet aggregation.     

Calcium mobilization by the plant estrogen ferutinin does not induce blood platelet aggregation

Platelet activation is closely associated with an increase in intracellular Ca(2+) concentration. Various compounds including Ca(2+) ionophores are able to trigger platelet aggregation by increasing intracellular Ca(2+) concentration in platelets. In the present study, we monitored the effect of the phytoestrogen ferutinin, which acts as a Ca(2+) ionophore in human blood platelets; its ionophore-like properties include upregulation of [Ca(2+)](in), activation of fibrinogen receptors and increased fibrinogen binding. Using spectrofluorometry and triple-color flow cytometry, we demonstrate that ferutinin increases [Ca(2+)](in) in both isolated platelets and platelets in whole blood from humans. This effect was almost completely blocked by the Ca(2+) chelator EGTA and was not sensitive to either Gd(3+) or econazole, which inhibit VOC and SOC channels, respectively. Nor was the effect sensitive to thapsigargin, an inhibitor of endoplasmic reticulum Ca(2+) ATPases. Ferutinin stimulated the expression of the active form of the GPIIb-IIIa complex and whole blood platelet aggregation only weakly and had no statistically significant effect on the binding of fibrinogen. These results demonstrate apparently inconsistent effects of ferutinin, which raises intraplatelet Ca(2+) concentration but fails to have an effect on spontaneous blood platelet aggregation. This pattern of responses may be caused by the combination of ferutinin's Ca(2+) ionophoric and estrogenic properties.     

Ginkgolide C inhibits platelet aggregation in cAMP- and cGMP-dependent manner by activating MMP-9

In this report, we investigated the effect of ginkgolide C (GC) from Ginkgo biloba leaves in collagen (10 mug/ml)-stimulated platelet aggregation. It has been known that matrix metalloproteinase-9 (MMP-9) is released from human platelets, and that it significantly inhibited platelet aggregation stimulated by collagen. Zymographic analysis confirmed that pro-MMP-9 (92-kDa) was activated by GC to form an activated MMP-9 (86-kDa) on gelatinolytic activities. And then, GC dose-dependently inhibited platelet aggregation, intracellular Ca(2+) mobilization, and thromboxane A(2) (TXA(2)) formation in collagen-stimulated platelets. In addition, GC significantly increased the formation of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), which have an anti-platelet function in both resting and collagen-stimulated platelets. Therefore, we demonstrate that the inhibitory effect of GC on platelet aggregation might be involved into the following pathways. GC may increase intracellular cAMP and cGMP production and MMP-9 activity, inhibit intracellular Ca(2+) mobilization and TXA(2) production, thereby leading to inhibition of platelet aggregation. These results strongly indicate that GC is a potent inhibitor of collagen-stimulated platelet aggregation. It may be a suitable tool for a negative regulator during platelet activation.     

人精子膜的离子通道和男性抗生育中草药的避孕机制(英文)

利用离子通道-脂双层重组技术,即将分离的人精子通道蛋白重组于人工脂双层膜,利用膜片箝技术记录、分析通道性质的方法,已鉴定了人精子膜数种通透Ca~(2+)、K~+、Na~+和Cl~-通道的生物物理和药理学性质,提供了成熟精子离子通道的基本电生理资料。利用小鼠生精细胞和膜片箝技术分析棉酚及由避孕中药雷公藤分离的多种单体对Ca~(2+)通道的作用,发现它们均在抑制精子顶体反应的浓度水平上抑制T型Ca~(2+)通道,表明对Ca~(2+)通道的抑制与它们的避孕效应密切相关;观察药物对小鼠生精细胞Ca~(2+)通道的作用,是筛选抗生育化合物特别是局部急用避孕药的一个有效方法。     

库容性Ca~(2+)内流介导大鼠远端结肠平滑肌收缩

目的探讨库容性Ca2+内流(capac itative Ca2+entry,CCE)是否参与大鼠远端结肠平滑肌兴奋-收缩偶联过程。方法利用器官离体装置、张力换能器、Powerlab 4/25T数据采集分析系统测定远端结肠平滑肌的张力。结果毒胡萝卜素(thapsigargin,TG,10 nmol.L-1~1μmol.L-1)诱导结肠平滑肌条产生持续的张力性收缩,不同浓度TG所致的同步收缩反应张力不同。在无钙Krebs液(包含1 mmol.L-1EDTA)中使用TG将肌条培养35 m in后,再加入Ca2+2.5mmol.L-1,比未使用TG处理的肌条产生的收缩张力明显提高(99%±28%vs70%±8%)。且TG耗竭胞内钙库后再复钙所致的收缩效应,不受L型钙通道阻断剂verapam il影响,但可被SOC通道阻断剂La3+减弱。结论TG耗竭胞内钙库后再复钙诱导的大鼠远端结肠平滑肌收缩反应由CCE介导,提示CCE是提供大鼠远端结肠平滑肌收缩的激活信号Ca2+的来源之一,参与完成结肠平滑肌兴奋-收缩偶联过程。     

J—894对人体血小板激活时胞浆内游离钙浓度的影响

细胞内游离钙浓度在细胞反应的调节中作为第二信使起很重要的作用。本文实验采用荧光钙指示剂quin-2测定血小板胞浆内游离钙浓度[Ca^2 ]i的变化。结果表明在1mmol/L外钙的存在下，凝血酶（0.3U/ml）使血小板[Ca^2 ]i增高4－5倍。但在外钙缺乏的情况下，凝血酶使血小板[Ca^2 ]i增加较少，似科凝血酶增加[Ca^2 ]i，部分是通过释放内钙，但主要是通过钙内.J-894通过减少钙内流和释放明显抑制凝血酶引起的血小板[Ca^2 ]i的升高，剂量与效应相关。提示J－894可能是一种钙通道阻滞剂。     

杏花雨对外源性高钙致大鼠脑线粒体损伤的保护作用

目的探讨杏花雨注射液对外源性高钙所致线粒体损伤的保护作用.观察杏花雨对离体线粒体是否具有保护作用,从而进一步完善银杏叶提取物抗脑缺血损伤的机制.方法新鲜制备的大鼠脑线粒体悬液,分别与不同浓度Ca2 以及不同浓度的杏花雨注射液进行孵育,观察线粒体基质游离钙、线粒体活性以及线粒体膜肿胀度的变化.结果与正常对照组比较外源性高钙导致大鼠脑线粒体严重钙超载(P＜0.01),线粒体活性下降(P＜0.01),540 nm处线粒体悬液吸光度值显著下降,线粒体明显肿胀(P＜0.01);于钙离子损伤前给予杏花雨孵育,线粒体基质游离钙浓度明显降低(P＜0.01),线粒体活性显著升高(P＜0.01),吸光度值有明显升高,显示线粒体肿胀度减轻(P＜0.01).结论外源性高钙可使线粒体基质游离钙含量升高,产生线粒体通透性转换(mitochondria permeability transition,MPT),使线粒体活性降低,功能障碍.杏花雨通过缓解线粒体钙超载,防止产生MPT,从而恢复线粒体功能.提示杏花雨抑制线粒体钙超载可能是其对缺血再灌注脑损伤的保护作用机制.     

用Fura-2测定突触体内游离Ca2+浓度及Ca2+通道激动剂和阻断剂的影响

用Fura-2测定大鼠突触体内游离Ca²⁺浓度,探讨Ca²⁺通道激动剂和阻断剂对突触体内钙浓度的影响。测得突触体内Ca²⁺浓度为200～400 nmol/L。观察了不同浓度KCl,CaCl₂,NMDA和谷氨酸对突触体内Ca²⁺增加的影响以及维拉帕米及MgCl₂对KCl和NMDA引起钙内流的阻断作用。本实验提供一个研究突触体内Ca²⁺变化的准确而稳定的方法,并对测定中几个影响因素加以讨论。     

铅对大鼠脑突触体钙调素的抑制作用

用体外法,将大鼠脑突触体膜,在不同浓度的Pb~(2+)作用下分别测定CaM依赖的Ca~(2+)-ATP酶和CaM活性的IC_(50)值。结果表明,Pb~(2+)对Ca~(2+)-ATP酶活性IC_(50)为 1.62mM;对CaM活性IC_(50)为3.85mM。当向不含CaM的脑突触体加入3.0～10.0μg的外源性CaM后,被Pb~(2+)抑制的Ca~(2+)-ATP酶活性均有显著的逆转而恢复或接近正常水平。推测Pb~(2+)主要直接作用在脑突触体膜的CaM,通过CaM分子构象改变,抑制Ca~(2+)-ATP酶,这可能是铅神经毒性的分子基础。