牛心内膜腺苷三磷酸双磷酸酶对血小板聚集的抑制作用

AIM: To study the anti-aggregatory effect of bovine endocardial endothelial cell (EEC)-associated apyrase. METHODS: Cultured bovine EEC was used. Adenosine diphosphate (ADP) was analyzed by reversed phase HPLC, and rabbit platelet aggregation was measured turbimetrically. RESULTS: Incubation of EEC with ADP 500 mumol.L-1 resulted in a progressive decrease in ADP concentration, which was paralleled by the decrease in platelet aggregating potential of the unmetabolized ADP. In the presence of aspirin (Asp 1 mmol.L-1)-treated EEC 1 x 10(9) cells.L-1, the aggregation of Asp (1 mmol.L-1) and methylene blue (10 mumol.L-1)-treated platelets in response to thrombin 500 U.L-1 and platelet activating factor (PAF 1 nmol.L-1) was markedly inhibited and was reversible, which was very similar to that in apyrase-treated platelets. The supernatants of EEC had no effect on platelet aggregation. EEC inhibited ADP (5 mumol.L-1)-induced platelet aggregation, but failed to inhibit adenosine 5'-O-(2-thiodiphosphate) (ADP-beta-S, an unmetabolizable structural analog of ADP, 15 mumol.L-1)-induced platelet aggregation. CONCLUSION: ADP hydrolysis by EEC-associated apyrase is a major anti-thrombotic mechanism of bovine EEC.     

三七皂甙对心肌腺苷三磷酸酶的影响(英文)

三七总皂甙(PNS)能抑制心肌总ATP酶活力,但对Na~( )-K~( )-ATP酶无明显影响。三七皂甙单体Rb_1及Rg_1对心肌总ATP酶活力均有抑制作用,但Rb_1的抑制效力显著大于Rg_1·Rb_1能抑制豚鼠离体心房肌的自律性和收缩性,Rg_1也能抑制豚鼠离体心房肌的自律性,但对心房肌的收缩性却无明显影响。提示PNS抑制心肌收缩力这一作用的主要有效成份是Rb_1·     

槲皮素对大鼠钠钾腺苷三磷酸酶和钙镁腺苷三磷酸酶的影响(英文)

槲皮素(Que)ig 200mg·kg~(-1),qd×14d可显著降低大鼠心肌和脑钠钾腺苷三磷酸酶(Ⅰ)的活力及心肌钙镁腺苷三磷酸酶(Ⅱ)的活力;槲皮素100mg·kg~(-1)降低心肌Ⅰ的活力,但对脑Ⅰ无明显影响。实验结果提示,大鼠心肌Ⅰ对Que的反应较脑Ⅰ敏感;槲皮素也能显著抑制心肌Ⅱ的活力。     

三磷酸腺苷或腺苷对心律失常的诊疗作用

三磷酸腺苷或腺苷是临床诊疗心律失常的一种重要方法，它可终止阵发性室上性心动过速，终止特殊类型室速，对多种类型的心律失常有鉴别诊断作用。另外，三磷酸腺苷或腺苷对窦房结功能障碍也有诊断价值，还可应用于射频导管消融术。     

培养的牛心内膜内皮细胞水解细胞外腺苷酸

目的:研究牛心内膜内皮细胞(BEEC)腺苷三磷酸双磷酸酶(apyrase)的特性并比较牛心内膜及血管内皮细胞的胞外腺苷酸酶活性。方法:以反相HPLC测定核苷酸含量,以磷离子释放法检测apyrase活性。结果:叠氮钠10mmol·L~(-1)和氟化钠20mmol·L~(-1)分别抑制BEEC apyrase 51％及38％活性,而Na~ /K~ -ATP酶抑制剂哇巴因则对BEEC apyrase活性无影响。过氧化氢0.5mmol·L~(-1)呈时间依赖性地抑制心内膜内皮细胞apyrase活性。BEEC的apyrase活性低于主动脉内皮细胞的apyrase活性,而BEEC的胞外AMP酶则远较血管内皮细胞的活性高。结论:BEEC apyrase具有叠氮钠和氟化钠敏感的、哇巴因不敏感的特性;与血管内皮细胞相比,BEEC apyrase活性较高而胞外AMP酶活性较低。     

槲皮素对大鼠钠钾腺苷三磷酸酶和钙镁腺苷三磷酸酶的影响

槲皮素（Ｑｕｅ）ｉｇ２００ｍｇ．ｋｇ＾－１，ｑｄ×１４ｄ可显降低大鼠心肌和脑钠钾腺苷三磷酸酶的活力及心肌钙镁腺苷三磷酸酸的活力；槲皮素１００ｍｇ．ｋｇ＾－１降低心肌Ｉ的活力，但对脑Ｉ无明显影响。实验结果提示，大鼠心肌Ｉ对Ｑｕｅ的反应较脑Ｉ敏感；槲皮素也能显抑制心肌ＩＩ的活力。     

四氢小檗碱对血小板聚集和血栓形成的抑制作用(英文)

SD大鼠每天ip THB 30 mg·kg~(-1)共3 d或5 d后,使ADP诱导的血小板聚集程度降低;同剂量ip 1 d,3 d或5 d后,使AA诱导的血小板聚集程度降低,THB在体外抑制AA,ADP和胶原诱导的兔血小板聚集,IC_(50)分别为0.86,1.31和1.10 mmol·L~(-1) THB能抑制AA诱导的兔血小板生成血栓素B_2 THB 15—30 mg·kg~(-1)iv明显抑制大鼠静脉血栓的形成。     

三磷酸腺苷二钠HPLC检测的影响因素探讨

用HPLC法检测三磷酸腺苷二钠（ATP）含量时,因成品中的二磷酸腺苷二钠（ADP）及蛋白质在259nm附近都有紫外吸收，因此ADP和蛋白质对含量测定有一定的影响。经试验对上述两种因素的影响进行了初步探讨。结显示当ADP的峰面积小于5％，蛋白质杂志峰总面积小于1％时，对HPLC法测定ATP含量无影响。     

三七皂甙对心肌腺苷三磷酸酶的影响

三七总皂甙（ＰＮＳ）能抑制心肌总ＡＴＰ酶活力，但对Ｎａ＾（＋）－Ｋ＾（＋）－ＡＴＰ酶无明显影响。三七皂甙单体Ｒｂ１及Ｒｇ１对心肌总ＡＴＰ酶活力均有抑制作用。但Ｒｂ１的抑制效力显著在Ｒｇ１，Ｒｂ１能抑制豚鼠离体心房肌的自律性和收缩性。Ｒｇ１能抑制豚鼠体心房肌的自律性，但对心房肌的收缩性却无明显影响。提示ＰＮＳ抑制心肌收缩力这一作用的主要有效成份是Ｒｂ１。     

外源性三磷酸腺苷和腺苷对肿瘤细胞增殖的影响

目的　研究三磷酸腺苷 (ATP)和腺苷 (ADO)对人红白血病细胞株K5 6 2、人胃中分化腺癌细胞株HGC 2 7、人食管低分化鳞癌细胞株TE 13细胞增殖的影响。方法　采用MTT法测定ATP和ADO抑制肿瘤细胞增殖的作用 ,Wright’s Giemsa染色观察细胞形态学的改变。结果　在 0 0 1～ 1 0mmol·L-1浓度范围内 ,ATP和ADO可不同程度地抑制TE 13、HGC 2 7和K5 6 2细胞的增殖 ,其中对TE 13的作用最强 ;ATP和ADO作用 72h后 ,对TE 13细胞的抑制率分别为80 5 2 %和 74 0 3%。细胞经高浓度 (1mmol·L-1)的ATP和ADO处理后 ,细胞形态出现了凋亡的特征。结论　ATP抗TE 13和HGC 2 7肿瘤细胞增殖的作用与其代谢产物ADO部分相关 ,ATP和ADO的作用机制可能涉及细胞凋亡     

Platelet-released ADP stabilizes PAF-induced rabbit platelet aggregation by stabilizing intracellular calcium

ＰｌａｔｅｌｅｔｒｅｌｅａｓｅｄＡＤＰｓｔａｂｉｌｉｚｅｓＰＡＦｉｎｄｕｃｅｄｒａｂｂｉｔｐｌａｔｅｌｅｔａｇｇｒｅｇａｔｉｏｎｂｙｓｔａｂｉｌｉｚｉｎｇｉｎｔｒａｃｅｌｕｌａｒｃａｌｃｉｕｍ１ＹＩＦｕＸｉａｎ，ＧＵＯＺｈａｏＧｕｉ２（Ｌａｂ...     

Inhibition of platelet aggregation by adenosine receptor agonists

2-(Ar)alkoxyadenosines, which are agonists selective for the A_2AAR in PC 12 cell and rat striatum membranes, are also agonists at the A₂AR coupled to adenylate cyclase (AC) that mediates the inhibition of platelet aggregation. A panel of twelve well-characterized adenosine analogues stimulated human platelet AC and inhibited ADP-induced platelet aggregation at sub- to low-micromolar concentrations with a potency ranking CGS 21680 < adenosine < R-PIA. There were significant correlations between the ECso of anti-aggregatory activity and either the ECso of stimulation of platelet and PC 12 cell AC (r ² = 0.66 and 0.67, respectively) or the K₁ of inhibition of [³H]NECA binding to the rat striatum membranes (r ² = 0.75). Likewise, platelet AC stimulation correlated well with stimulation of PC 12 cell AC and with [³H]NECA binding (r ² = 0.94 and 0.91, respectively). Ten 2-(ar)alkoxyadenosines stimulated platelet AC at EC₅₀s ranging between 0.16 and 2.3 μM and inhibited platelet aggregation at EC₅₀s ranging between 2 and 30 μM. There were no correlations between the EC₅₀s of anti-aggregatory activity and either the EC₅₀s of the stimulation of platelet or PC 12 AC (r ² = 0.08 and 0.06, respectively) or with the K₁ of the inhibition of [³H]NECA binding to the A_2aAR in rat striatum (r ² = 0.02). The EC₅₀s of the stimulation of platelet AC correlated with those of the stimulation of PC 12 AC (r ² = 0.48), and also with the K₁ of [³H]NECA binding (r ² = 0.71). Each of the 23 adenosines completely inhibited platelet aggregation and thus, functionally, all behaved as full agonists. As stimulants of PC 12 cell AC, Group A and B analogues were equally efficacious. As stimulants of platelet AC, however, the efficacy relative to NECA ( = 1.0) of Group B analogues was significantly less than that of Group A analogues, 0.49 ± 0.2 vs. 0.72 ± 0.05, P±0.01. The partial agonist activity of Group B analogues at the platelet A2AR but full agonist activity at the PC 12 cell A_2aAR, as well as the relatively low correlations between platelet AC stimulation and other indices of A_2aAR agonist actlVlty, suggest the platelet receptor is not a typical A_2aAR. Further, the lack of a correlation between the platelet anti-aggregatory and AC stimulatory activity suggests that (a) the 2-(ar)alkoxyadenosines might affect platelet aggregation by mechanisms other than AC stimulation or (b) that the stimulation of the platelet membrane AC by 2-(ar)alkoxy-adenosines does not correspond to the accumulation of cyclic AMP in intact platelets.     

槲皮素对氧自由基诱发血小板聚集性变化的影响(英文)

目的:观察氧自由基对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Born'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))和氢化可的松(900mg·L~(-1))在体外均可明显地清除氧自由基,使发光强度分别下降75.7％和79.0％。结论:氧自由基参与了血小板聚集过程,槲皮素对氧自由基的清除作用是其抑制血小板聚集的又一作用机制。     

Inhibitory effects of copper-aspirin complex on platelet aggregation

目的：研究阿司匹林铜（ＣｕＡｓｐ）对血小板聚集性的影响及其机制．方法：用Ｂｏｒｎ氏法测定ＣｕＡｓｐ对兔血小板聚集性的影响．用荧光光度法和放射免疫法观察ＣｕＡｓｐ对兔血小板５羟色胺的释放和ＴＸＢ２的产生及血浆中ＴＸＢ２和６ｋｅｔｏＰＧＦ１α水平的影响．结果：ＣｕＡｓｐ体外呈浓度依赖性抑制花生四烯酸（ＡＡ）诱导的血小板聚集和５羟色胺的释放（ＩＣ５０分别为１７和１９μｍｏｌ·Ｌ－１，９５％可信限为９－３３和１０－３０μｍｏｌ·Ｌ－１），且抑制ＴＸＢ２的产生（Ｐ＜００５）．ＣｕＡｓｐ１０ｍｇ·ｋｇ－１灌胃选择性抑制ＡＡ诱导聚集．降低血浆ＴＸＢ２，同时升高６ｋｅｔｏＰＧＦ１α的水平（Ｐ＜００５）．结论：ＣｕＡｓｐ体内外均有比Ａｓｐ更强的抗血小板聚集作用．     

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。     

烙铁头蛇毒血小板聚集素对血小板聚集和抑制剂关系的研究

研究山莨菪碱(654-2)、阿斯匹林(ASA)、前列环素(PGI_2)样物质对二磷酸腺苷(ADP)、花生四烯酸(AA)以及烙铁头蛇毒血小板聚集素(TMVA)诱导的阻抗法全血血小板聚集(简称全血聚集)的影响。结果表明:ADP.AA.TMVA诱导的全血聚集随剂量增加而增强.阻抗技术对于估价生理条件下的血小板功能较为敏感。654-2促进ADP诱导的全血聚集.而ASA和PGI_2样物质对ADP和AA诱导的聚集均有抑制作用.但不能防止TMVA诱导的聚集。提示TMVA可能通过第3途径(类似于血小板活化因子.PAF)诱导血小板聚集.经ADP和AA作用过的血小板对TMVA的活化仍有反应,其机理值得研究。     

烟酰水杨酸对Collagen、ADP、AA诱导的兔血小板聚集的影响

目的观察烟酰水杨酸(NSA)对Collagen、ADP、AA诱导的兔血小板聚集的影响。方法用比浊法测定了NSA体外、体内对兔血小板聚集的影响。结果NSA能明显抑制体外、体内Collagen、ADP诱导的血小板聚集,体外最大抑制率分别为55.7%、61.3%,体内最大抑制率分别为42.2%、74.8%。NSA对AA诱导的兔血小板聚集没有影响。结论NSA具有抑制Collagen、ADP诱导的血小板聚集的作用。其抑制作用具有明显的量效关系。