水杉总黄酮对高脂血症大鼠血小板聚集、释放功能及超微结构的影响

目的:研究水杉总黄酮(FMG)对高脂血症大鼠血小板聚集、释放功能及超微结构的影响.方法:CHOD-PAP法和GPO-PAP法测定血浆胆固醇和三酰甘油含量、比浊法测定血小板聚集率、双抗夹心免放法测定血浆GMP-140含量、硝酸还原酶法和分光光度法测定血小板NO含量和NOS活性,并观察血小板超微结构.结果:FMG降低高脂血症大鼠血浆胆固醇、三酰甘油水平、血小板最大聚集率、血浆GMP-140含量,提高血小板NO含量和NOS活性,减轻血小板超微结构的损伤程度.结论:FMG能降低高脂血症大鼠血浆脂质含量,抑制其血小板聚集、释放功能,激活血小板内L-Arg/NO途径,减轻血小板损伤程度.     

葛根素注射液对急性血淤模型大鼠血液流变学及血小板聚集的影响

目的:观察葛根素注射液对急性血淤模型大鼠血小板聚集的影响。方法:给大鼠注射大剂量盐酸肾上腺素和施以冰水浸 泡,制作急性血淤模型大鼠;采用全自动血流变学仪测定不同切变率的全血粘度、血浆粘度、血液屈服应力和红细胞聚集指数等指 标;以比浊法测定各组的血小板最大聚集率。结果:急性血淤模型大鼠的血液流变性呈异常改变,血小板聚集明显增高,葛根素注 射液对异常改变的血流变学和血小板聚集均有明显的改善作用。结论:葛根素注射液可明显改善急性血淤模型大鼠的血液流变学 作用和抑制异常增高的血小板聚集功能,且呈现一定的量效关系。     

精氨酰-谷氨酸二肽的抗血小板、抗凝活性和作用机制

目的　观察左旋精氨酰 谷氨酸二肽 (L Arg Glu)对大鼠血小板聚集、血栓形成、血液流变性、凝血纤溶系统及血浆NO、cGMP、PGI2 的影响。方法　 2 4只SD大鼠随机分为3组 ,分别灌服阿斯匹林 36mg·kg-1·d-1,Arg Glu 6 1.4mg·kg-1·d-1及同体积对照液 ,8d后检测血流变、凝血纤溶指标 ;2 4只SD大鼠随机分为 2组 ,处理相同 ,比浊法测定血小板聚集活性 ,放免法测定血浆cGMP、PGI2 水平 ,分光光度法测定一氧化氮浓度 ;另 2 4只SD大鼠分为两组 ,处理相同 ,以颈总动脉 颈外静脉旁路模型观察血栓湿重。结果　L Arg Glu与对照组相比可明显降低全血表观黏度、还原黏度、红细胞压积和血浆黏度 ,延长血浆复钙时间、白陶土部分凝血活酶时间及凝血酶原时间 (P <0 0 5 ) ,可使大鼠血小板聚集活性降低 (ADP及AA诱导 ) ,血栓湿重降低 ,血浆NO和cGMP升高 ,PGI2 有升高趋势 ,但差异无统计学意义。结论　Arg Glu二肽有抗血栓、改善血液流变性、抑制血小板聚集活性 ,可视为一NO前体 ;其作用机制推测除可能由精氨酸 一氧化氮 环磷酸鸟苷酸代谢通路 (Arg NO cGMPpathway)所介导外 ,尚有其它作用机制参与。     

葛根素对大鼠血瘀证模型血细胞聚集作用的研究

目的　探讨葛根素对急性血瘀证模型大鼠血细胞聚集的改善作用。方法　采用反复注射肾上腺素和施以冰水浸泡的方法制作急性血瘀证大鼠模型,以全自动血流变学仪测定全血粘度和红细胞聚集指数等指标,以比浊法测定血小板最大聚集率。结果　急性血瘀证模型大鼠的血液粘度显著升高,同时红细胞聚集功能和血小板聚集率明显增强;葛根素注射液对急性血瘀证导致的异常改变的血液粘度、红细胞聚集功能和血小板聚集率均有明显的改善作用。结论　葛根素具有明显改善急性血瘀证模型大鼠异常的血液流变学状态,明显抑制其异常增高的血细胞聚集作用,且呈现一定的量效关系。     

葛根素对大鼠血瘀证模型血细胞聚集作用的研究

目的探讨葛根素对急性血瘀证模型大鼠血细胞聚集的改善作用。方法采用反复注射肾上腺素和施以冰水浸泡的方法制作急性血瘀证大鼠模型，以全自动血流变学仪测定全血粘度和红细胞聚集指数等指标，以比浊法测定血小板最大聚集率。结果急性血瘀证模型大鼠的血液粘度显著升高，同时红细胞聚集功能和血小板聚集率明显增强；葛根素注射液对急性血瘀证导致的异常改变的血液粘度、红细胞聚集功能和血小板聚集率均有明显的改善作用。结论葛根素具有明显改善急性血瘀证模型大鼠异常的血液流变学状态，明显抑制其异常增高的血细胞聚集作用，且呈现一定的量效关系。     

红花对急性血瘀模型大鼠的活血化瘀作用研究

目的:通过药效学指标检测,评价红花在活血化瘀方面的作用。方法:42只大鼠分为空白组、模型组、阿司匹林治疗组(15 mg·kg~(-1))、红花低、中、高剂量组(1000、2000、4000 mg·kg~(-1)),采用皮下注射肾上腺素结合冰水游泳复制大鼠急性血瘀模型,测定各组大鼠的血液流变学指标、凝血参数、血小板聚集率、血浆6-keto-PGF1α、血栓素B_2(TXB_2)和内皮型一氧化氮合酶(eNOS)含量。结果:红花高中低剂量组能不同程度降低血小板聚集率,延长凝血酶原时间(PT)和活化部分凝血酶原时间(APTT),降低全血粘度(WBV)、血浆粘度(PV),升高血清eNOS、6-keto-PGF1α,降低TXB_2含量等。结论:红花通过恢复血小板聚集活性、改善凝血功能、血液流变性、血管内皮功能,抑制血栓形成等途径,对大鼠急性血瘀有较好的保护和治疗作用     

祛瘀宁痛贴治疗急性软组织损伤的机理探讨

目的 :探讨祛瘀宁痛贴治疗急性软组织损伤的作用机理。方法 :采用大鼠急性软组织损伤模型 ,观察祛瘀宁痛贴对大鼠血液流变学指标、血小板聚集率和血栓形成的影响。结果 :祛瘀宁痛贴 0 .3、0 .9、1.8g·kg-1生药能明显降低急性软组织损伤大鼠的全血粘度、血浆粘度、纤维蛋白原含量、红细胞压积 ,减慢血沉速度 ,降低血沉K值 ,缩短红细胞电泳时间 ,并能抑制血小板聚集率和体外血栓形成 (P<0 .0 5或P <0 .0 1)。结论 :改善血液流变学 ,抑制血小板聚集和血栓形成 ,可能是祛瘀宁痛贴治疗急性软组织损伤作用机理的一方面。     

虎杖苷降低急性血瘀模型大鼠血液粘度的研究

目的 :探讨虎杖苷降低急性血瘀模型大鼠血液粘度的作用。方法 :采用大鼠急性血瘀模型 ,以全血高切变率及低切变率粘度值、红细胞压积值、血小板粘附率、纤维蛋白原含量、血浆粘度为观察指标。结果 :虎杖苷可以显著降低模型大鼠的纤维蛋白原含量和血小板粘附率 ,其药效对血浆粘度降低所致全血粘度降低比其它原因所致更显著 ,它主要通过降低血浆粘度来降低全血粘度 ,从而显著改善大鼠血液循环。结论 :虎杖苷对血液粘度降低有重要应用价值。     

淫羊藿总黄酮对家兔血液流变性及血小板聚集的影响

目的:探讨淫羊藿总黄酮对家兔血液流变性及血小板聚集的影响。方法:测定淫羊藿总黄酮灌胃给药对家兔血黏度和血小板聚集的影响。结果:淫羊藿总黄酮灌胃30~120mg·kg-1可显著降低家兔全血黏度、红细胞压积和红细胞聚集指数;抑制腺苷二磷酸诱导的家兔血小板聚集。结论:淫羊藿总黄酮具有改善家兔血液流变性、血小板聚集作用。     

天舒滴丸对急性血瘀模型大鼠血液流变学和血栓形成的影响

目的研究天舒滴丸对急性血瘀模型大鼠血液流变学、血小板聚集及血栓形成的影响。方法 SD大鼠随机分为对照组、模型组、天舒胶囊(4.0 g/kg)组、天舒滴丸(1.0、2.0、4.0 g/kg)组,ig给药3 d后,采用肾上腺素配合冰浴制备大鼠急性血瘀模型,分别测定全血黏度,血浆黏度,红细胞压积,血沉,体外形成血栓的长度、湿质量、干质量,血小板聚集率等指标。结果天舒滴丸能明显降低急性血瘀模型大鼠全血和血浆黏度,明显降低血栓长度、血栓湿质量和干质量,抑制模型大鼠血小板聚集率的升高。结论天舒滴丸能够改善急性血瘀模型大鼠血液流变性,抑制血小板聚集及血栓形成。     

5-Hydroxytryptamine and thromboxane in platelets from rats treated with monocrotaline pyrrole

Monocrotaline pyrrole (MCTP), a metabolite of the plant toxin monocrotaline, produces pulmonary vascular injury, pulmonary hypertension, and right ventricular enlargement (RVE) in rats by an unknown mechanism. A role for platelets has been suggested by the observation that antibody-induced thrombocytopenia reduces the RVE caused by MCTP. The platelet can release a number of vasoconstrictive agents, such as 5-hydroxytryptamine (5HT) and thromboxane A2 (TxA2), that could possibly contribute to pulmonary hypertension. It was of interest to determine whether treatment with MCTP alters platelet 5HT content or alters the release of TxA2 in platelet-rich plasma (PRP) in response to aggregation. Fourteen days following treatment with MCTP when pulmonary hypertension is well-established and RVE is present, the concentration of 5HT in washed platelets or in platelet-poor plasma was not different in treated and control rats. One day following treatment with MCTP, before lung injury is evident, the concentration of TxB2, a stable metabolite of TxA2, was higher in unstimulated PRP from treated rats than in control rats. The concentration of TxB2 was also examined in PRP at 4 days (when lung injury first appears), 7 days (when pulmonary arterial pressure first increases), and 14 days after treatment with MCTP (when RVE is evident). At 4, 7, or 14 days following treatment there was no difference in the concentration of TxB2 in unstimulated PRP from MCTP-treated and control rats. Following stimulation with arachidonic acid, the release of TxB2 at maximal aggregation was not different in PRP from MCTP-treated and control rats at any time after treatment. The rate of release of TxB2 was lower in PRP from rats treated with MCTP 7 days earlier, but was not different at any other time following treatment. At concentrations up to 250 micrograms/ml, MCTP added in vitro to PRP from untreated rats did not affect the concentration of TxB2 released during aggregation induced by arachidonic acid. Only at very high concentrations (1 mg/ml) did MCTP abolish the aggregation response and depress TxB2 release in PRP. These results indicate that MCTP treatment does not affect platelet 5HT content and does not affect basal TxB2 production or TxB2 release by platelets stimulated in vitro.     

Inhibition of platelet-derived mitogen release by nitric oxide (EDRF)

Platelets exposed to thrombogenic surfaces adhere, aggregate and release mitogenic substances from their alpha-granules. Endothelium-derived relaxing factor (EDRF) which has been identified as nitric oxide (NO) has been reported to inhibit platelet aggregation. We now report that NO inhibits mitogen release from stimulated human platelets. Mitogenic activity was assayed on mouse fibroblast 3T3 cells using incorporation of 3H-thymidine. Serum from collagen-aggregated platelets significantly increased 3H-thymidine incorporation by 3T3 cells above that of serum from control platelets. Both this increase and platelet aggregation were blocked by NO and prostacyclin in a dose related manner. The inhibitory activity of NO decayed with time when incubated in platelet-free plasma at 37 degrees C, but was still detectable after 2 minutes.     

蝙蝠葛酚性碱对血栓形成和血小板聚集的影响蝙蝠葛酚性碱对血栓形成和血小板聚集的影响

目的观察蝙蝠葛酚性碱(PAMD)对血栓形成、血小板聚集的影响并研究其作用机制。方法用动静脉短路血栓形成模型观察血栓形成；比浊法测定血小板聚集度；电镜技术观察血小板超微结构变化；放射免疫法测定TXB₂和6-酮基-PGF1α的水平；硝酸还原酶法测定兔血浆NO浓度。结果PAMD体内给药可剂量依赖性地抑制血栓形成及由ADP，AA和THR诱导的大鼠和兔的血小板的聚集；可显著抑制血小板超微结构的变化；能明显升高兔血管壁6-酮基-PGF1α产生量，对血小板释放的TXB₂无明显影响；还可提高兔血浆NO的浓度。结论PAMD具抗血栓形成和抗血小板聚集的作用，其机制与增加血管壁PGI₂含量，提高兔血浆NO的浓度有关。     

川芎嗪对大鼠脑梗塞的保护作用

目的　研究川芎嗪（ｌｉｇｕｓｔｒａｚｉｎｅ,Ｌｉｇ） 对脑梗塞的保护作用。方法　大鼠脑梗塞模型采用右侧颈总动脉和右侧大脑中动脉的结扎,脑梗塞重量用ＮＢＴ 染色法测定。小鼠双侧颈总动脉结扎４ ｈ 后,取脑测丙二醛（ ＭＤＡ）、一氧化氮（ＮＯ）含量。血小板聚集用Ｂｏｒｎ 法测定。结果　Ｌｉｇ １０ ,２０,４０ ｍｇ·ｋｇ－ １ｉｖ 可显著改善大鼠异常神经症状和抑制ＡＬＰ活性的下降;Ｌｉｇ 可显著降低小鼠缺血脑组织ＮＯ 和ＭＤＡ 含量;Ｌｉｇ（２００,４００ ,８００ ｍｇ·Ｌ－１） 可显著抑制ＡＤＰ致血小板的聚集。结论　Ｌｉｇ 对脑梗塞有保护作用,此作用可能与抑制血小板聚集有关     

白藜芦醇对高脂血症大鼠血小板聚集的影响及其机制研究

目的:研究白藜芦醇对高脂血症大鼠血小板聚集的影响及其可能机制.方法:建立大鼠的高脂血症模型,同时连续i.g.给予白藜芦醇(50mg· kg-1·d-1)或空白溶媒30 d,测定大鼠血浆TC、TG、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、丙二醛(MDA)、超氧化物歧化酶(SOD)、NO、内皮一氧化氮合酶(eNOS)、p-选择蛋白、血栓烷B2 (TXB2)和6-酮-前列腺素F1α(6-Keto-PGF1α),ADP诱导的血小板5 min最大聚集率.结果:与高脂模型组比较,高脂饲料白藜芦醇组大鼠在连续i.g.给予白藜芦醇(50 mg·kg-1·d-1)30 d后,大鼠血浆TG、TC、LDL-C含量均下降,分别下降19％、31％、51％,HDL-C含量增加1.33倍;SOD和eNOS活力升高,NO和6-Keto-PGF1α含量增加,MDA、p-选择蛋白、TXB2含量降低,ADP诱导的血小板5 min最大聚集率降低.结论:白藜芦醇能有效降低血小板聚集,可能是通过降低血脂水平,防止脂质过氧化和保护内皮细胞完整,影响NO合成,维持血浆或组织中的TXA2和PGI2平衡及细胞内外的钙离子平衡等多环节来发挥作用.     

Inhibition of platelet aggregation by polyaspartoyl L-arginine and its mechanism

AIM: To observe the oral anti-platelet efficacy and the potential action mechanism of polyaspartoyl L-arginine (PDR), a new L-arginine rich compound. METHODS: Platelet aggregation was conducted by Born's method; bleeding time was determined using tail's bleeding time in mice; platelet adhesion was carried out with glass bottle method; nitric oxide (NO) was tested with Griess's method; and cAMP, thromboxane B(2) (TXB(2)) and 6-keto-PGF(1 alpha ) were assessed with commercial kits. RESULTS: The inhibition by PDR (15-60 mg/kg i.g. or 10 mg/kg i.v.) of platelet aggregation induced by adenosine diphosphate (ADP), collagen or thrombin at 1 h after oral administration or at 20 min after i.v. injection for rats (P<0.01), and its (15 mg/kg, i.g.) inhibition of ADP-induced platelet aggregation for rabbits during 6 h after administration were observed. PDR (15-60 mg/kg) prolonged the bleeding time of mice (P<0.05) and (30 mg/kg) increased NO concentration in plasma. On the other hand PDR did not change the contents of cAMP in platelet and TXB2 or 6-keto-PGF(1 alpha) in plasma. CONCLUSION: PDR is a novel, oral effective platelet aggregation inhibitor and its action mechanism possibly related to increasing NO generation.     

Interactions of ethanol with ionophore A23187 in human platelets and erythrocytes and in rat brain slices

The aggregation of gel-filtered human platelets induced by A23187 is very sensitive to inhibition by ethanol. Similarly when platelets preloaded with [3H]5-hydroxytryptamine ([3H]5HT) are studied in a superfusion system under conditions where aggregation is likely (high platelet density, presence of Ca2+) the rate of release of [3H]5HT induced by A23187 is reduced by the presence of ethanol. However when platelet aggregation is less likely (low platelet density, absence of Ca2+) ethanol does not reduce the rate of [3H]5HT efflux induced by A23187 in superfused platelets. In addition, in contrast to the effects of ethanol on platelet aggregation, the transformation of human red cells to echinocytes induced by A23187 is accelerated by the presence of ethanol. Similarly the increased efflux of 3H from superfused rat striatal slices preloaded with [3H]dopamine which is produced by A23187 is potentiated by ethanol. It is concluded that the inhibitory effect of ethanol on the action of A23187 may be confined to platelet aggregation. This may be because the mechanisms of action of either A23187 or ethanol on platelet aggregation differ from those on other cell functions.     

The effect of ethanol on some serotonergic mechanisms in rat blood platelets

Under in vitro conditions ethanol inhibits the uptake and enhances release of [14C]-5HT from rat blood platelets. Similar results were obtained in blood platelets isolated from the blood rats receiving 2 g/kg ethanol. Ethanol decreased also the 5-HT content in the blood platelets. It inhibited the aggregation of blood platelets but did not change the potentiating action of 5-HT on ADP-induced aggregation. The results indicate that ethanol by its action on the transport mechanisms in blood platelets may elevate the level of free 5-HT in the blood plasma, in this manner potentiating the action of the amine in the circulatory system.     

心绞痛患者血小板功能改变及丹参对其影响

本实验观察了心绞痛患者血小板环核苷酸水平,血浆TXB_2、6酮PGF_(10)深度、血小板内外5—HT含量及血小板聚集性的变化以及丹参治疗前后各指标的改变。结果表明,心绞痛患者血小板聚集性血浆5—HT和血浆TXB_2水平明显增高,而血小板内5—HT、血浆6—酮—PGF_(10)水平则明显低于对照组。丹参能增加血小板内cAMP水平,降低血浆5—HT水平,对血小板聚集性有抑制作用。     

Attenuation by prolonged nitric oxide synthase inhibition of the enhancement of fibrinolysis caused by environmental stress in the rat.

1. Nitric oxide (NO) suppresses platelet aggregation and plasminogen activator inhibitor (PAI) release from platelets, playing physiological and/or pathological roles in the haemostatic system. We investigated the effect of NG-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor, on the disseminated intravascular coagulation (DIC)-like phenomena in rats under environmental stress, induced by prolonged fluctuation in air temperature, known as SART (specific alternation of rhythm in temperature) stress. 2. Exposure of rats to SART stress for 7 days caused mild DIC-like symptoms such as thrombocytopenia, hypofibrinogenemia, decreased factor VIII: coagulant activity and shortened euglobulin clot lysis time (ECLT). The enhanced fibrinolysis was accompanied by a marked decrease in the activity of plasma PAI. 3. L-NAME, but not its D-enantiomer, when administered orally at 0.3-10 mg kg-1, twice a day for 7-day exposure to stress, inhibited the stress-induced decrease in fibrinogen levels in a dose-dependent manner, whereas it failed to alter platelet count, factor VIII:coagulant activity and plasma protein levels in stressed rats. All these parameters in unstressed rats were resistant to L-NAME at 10 mg kg-1. 4. Repeated treatment with 10 mg kg-1 of L-NAME blocked the shortening of ECLT and the decrease in PAI activity following stress exposure, although it was without effect in unstressed rats. 5. The inhibitory effects of L-NAME at 10 mg kg-1 on the stress-induced alterations in fibrinogen levels and in ECLT were significantly reduced by coadministered L-arginine at 1000 mg kg-1. 6. These findings demonstrate that repeated administration of L-NAME attenuates the enhanced fibrinolysis, without aggravating thrombocytopenia, in SART-stressed rats. Endogenous NO appears to contribute to the stress-induced development of fibrinolysis by suppressing, plasma PAI activity, most probably as a result of inhibition of the PAI release from platelets.