Cov khoom

1.To soj ntsuam seb adenosine diphosphate (ADP)-derived adenosine yuav inhibit platelet aggregation, tshwj xeeb tshaj yog nyob rau hauv lub xub ntiag ntawm P2Y₁₂ antagonist, qhov twg cov teebmeem ntawm ADP ntawm P2Y₁₂ receptor yuav tiv thaiv.Platelet aggregation tau ntsuas nyob rau hauv cov lus teb rau thrombin. peptide los ntawm platelet suav hauv platelet-nplua nuj plasma (PRP) thiab tag nrho cov ntshav nyob rau hauv lub xub ntiag ntawm ADP thiab P2Y₁₂ antagonists cangrelor, prasugrel active metabolite, thiab ticagrelor.Nyob rau hauv lub xub ntiag ntawm P2Y₁₂ antagonist, preincubation ntawm PRP nrog ADP inhibited aggregation;Cov nyhuv no tau raug tshem tawm los ntawm adenosine deaminase.Tsis muaj kev cuam tshuam ntawm kev sib sau ua ke tshwm sim hauv cov ntshav tag nrho tshwj tsis yog thaum dipyridamole tau ntxiv rau inhibit adenosine uptake rau hauv erythrocytes.Cov teebmeem ntawm ADP hauv PRP thiab tag nrho cov ntshav tau rov ua dua siv adenosine thiab tau ncaj qha ntsig txog kev hloov pauv hauv cAMP (kev soj ntsuam los ntawm vasodilator-stimulated phosphoprotein phosphorylation).Tag nrho cov txiaj ntsig yog tib yam tsis hais txog P2Y₁₂ antagonist siv.ADP inhibits platelet aggregation nyob rau hauv lub xub ntiag ntawm P2Y₁₂ antagonist los ntawm kev hloov mus rau adenosine.Inhibition tshwm sim hauv PRP tab sis tsis nyob rau hauv tag nrho cov ntshav tsuas yog thaum inhibited adenosine uptake.Tsis muaj leej twg ntawm P2Y₁₂ antagonists tau kawm replicated cov teebmeem ntawm dipyridamole hauv cov kev sim uas tau ua.

2.ADP raug suav hais tias yog ib qho tsis muaj zog platelet agonist vim yog cov lus teb tsis muaj kev sib sau ua ke nws induces hauv vitro ntawm physiological concentrations ntawm extracellular Ca(2+) [(Ca(2+) )(o)].Kev txo qis [Ca(2+)](o) paradoxically txhim kho ADP-evoked aggregation, ib qho txiaj ntsig uas tau raug ntaus nqi los txhim kho thromboxane A(2) ntau lawm.Txoj kev tshawb no tau tshuaj xyuas lub luag haujlwm ntawm ectonucleotidases hauv [Ca(2+)](o) -dependence ntawm platelet activation.Txo [Ca(2+)](o) los ntawm millimolar mus rau micromolar qib hloov ADP (10 μmol / l)-evoked platelet aggregation los ntawm ib ntus mus rau cov lus teb nyob rau hauv ob qho tib si platelet-nplua nuj plasma thiab ntxuav suspensions.Thaiv thromboxane A(2) ntau lawm nrog tshuaj aspirin tsis muaj kev cuam tshuam rau qhov no [Ca(2+)](o) -dependence.Kev tiv thaiv ntawm ADP degradation tshem tawm qhov sib txawv ntawm qhov qis thiab lub cev muaj zog [Ca(2+)](o) ua rau muaj kev sib koom ua ke ruaj khov thiab ruaj khov hauv ob qho tib si.Kev ntsuas ntawm extracellular ADP qhia txo qis degradation hauv cov ntshav thiab apyrase-muaj g saline ntawm micromolar piv rau millimolar [Ca(2+)](o).Raws li tau tshaj tawm yav dhau los, thromboxane A(2) tiam tau txhim kho ntawm qis [Ca(2+)](o), tab sis qhov no yog ywj siab ntawm ectonucleotidase kev ua (.) P2Y receptor antagonists cangrelor thiab MRS2179 qhia qhov tsim nyog ntawm P2Y(12) receptors. rau kev txhawb nqa ADP-evoked aggregation, nrog rau lub luag haujlwm me me rau P2Y(1).Hauv kev xaus, Ca(2+) -dependent ectonucleotidase kev ua haujlwm yog ib qho tseem ceeb uas txiav txim siab qhov twg ntawm platelet aggregation rau ADP thiab yuav tsum tau tswj rau hauv kev tshawb fawb ntawm P2Y receptor activation.