Argipressin acetate hmoov, molecular mis C46H65N15O12S2, molecular hnyav 1084.24 g / mol, tshwm raws li ib tug dawb mus tawm dawb crystalline hmoov, nrog ib tug pH nqi ntawm txog 3.5 thiab ib tug optical rotation ntawm -23.822℃(nyob rau hauv 1 mol / dm ³ acetic acid tov). Nws solubility yog zoo heev, nrog ib tug solubility ntawm ntau tshaj los yog sib npaug rau 360 mg / mL (332.03 mM) nyob rau hauv dej ntawm chav tsev kub. Kev cia khoom yuav tsum tau tswj nruj me ntsis ntawm 2-8℃kom tsis txhob degradation. Cov tshuaj no tsim cov qauv cyclic los ntawm disulfide bonds (Cys ¹ - Cys ⁶), nrog rau cov amino acid sequence ntawm H-Cys-Tyr-Phe-Gln-Asn-Cys{{25}, Gln-Asn-Cys{{25} qhov twg 8th arginine residue yog lub hauv paus ntawm nws lub npe. Nws muaj cov nyhuv antidiuretic ncaj qha rau lub raum, tuaj yeem cog lus nyob ib puag ncig sanguis hlab ntsha, thiab ua rau cov hnyuv, gallbladder, thiab zais zis. Tab sis arginine vasopressin yuav luag tsis cuam tshuam rau kev ua haujlwm.
Peb cov khoom
Argipressin Acetate COA
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| Certificate of Analysis | ||
| Compound npe |
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| Qib | Pharmaceutical qib | |
| CAS Nr. | 129979-57-3 | |
| Ntau | 80g | |
| Ntim txheem | PE hnab + Al foil hnab | |
| Chaw tsim tshuaj paus | Shaanxi BLOOM TECH Co., Ltd | |
| Ntau No. | 202501090053 | |
| MFG | Peb 9, 2025 | |
| EXP | Peb 8, 2028 | |
| Qauv |
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| Yam khoom | Enterprise txheem | Kev txheeb xyuas qhov tshwm sim |
| Qhov tshwm sim | Dawb los yog yuav luag dawb hmoov | Ua raws |
| Cov ntsiab lus dej | Tsawg dua lossis sib npaug li 5.0% | 0.45% |
| Poob rau ziab | Tsawg dua lossis sib npaug li 1.0% | 0.53% |
| Hnyav Hlau | Pb Tsawg dua lossis sib npaug li 0.5ppm | N.D. |
| Tsawg dua lossis sib npaug li 0.5ppm | N.D. | |
| Hg Tsawg dua lossis sib npaug li 0.5ppm | N.D. | |
| Cd Tsawg dua lossis sib npaug li 0.5ppm | N.D. | |
| Purity (HPLC) | Ntau dua lossis sib npaug li 99.0% | 99.90% |
| Ib qho impurity | <0.8% | 0.25% |
| Tag nrho microbial suav | Tsawg dua lossis sib npaug li 750cfu / g | 80 |
| E. Coli | Tsawg dua lossis sib npaug li 2MPN / g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (los ntawm GC) | Tsawg dua lossis sib npaug li 5000ppm | 400ppm ua |
| Cia | Khaws rau hauv qhov chaw kaw, tsaus, thiab qhuav hauv qab -20 degree | |
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| Tshuaj Formula: | C48H69N15O14S2 |
| Exact Mass: | 1127 |
| Molecular Luj: | 1128 |
| m/z: | 1127 (100.0%), 1128 (51.9%), 1129 (13.2%), 1129 (9.0%), 1128 (5.5%), 1130 (4.7%), 1129 (2.9%), 1129 (2.7%), 1128 (1.6%), 1130 (1.4%), 1130 (1.4%), 1131 (1.2%) |
| Elemental Analysis: | C, 51.10; H, 6.16; N, 18.62; O, 18.43; S, 5.68 |
Argipressin acetate hmoovyog ib qho khoom siv hluavtaws zoo ib yam li ntuj arginine vasopressin, uas hloov cov qauv ntawm cov tshuaj hormones ntuj los ntawm kev tshem tawm ib qho amino acid thiab hloov nws nrog cov amino acid sib txawv ntawm lwm txoj haujlwm. Cov tshuaj no tuaj yeem pab tswj cov ntshav los ntawm kev cuam tshuam rau qib coagulation yam VIII thiab Von Willebrand yam hauv sanguis, thiab tuaj yeem txhim kho qee yam ntawm cov tsos mob nocturia. Cov tshuaj no tsuas yog siv los kho cov tsos mob xws li mob ntshav qab zib insipidus, nocturnal enuresis, thiab hemophilia, thiab tseem tuaj yeem siv los ntsuas lub peev xwm ntawm lub raum kom pom cov zis.
Hemostatic nyhuv: kho cov kab mob hemorrhagic
Esophageal variceal rupture thiab los ntshav:
Esophageal variceal bleeding is one of the most serious complications of portal hypertension in liver cirrhosis. Its pathogenesis is the continuous increase of portal vein presure (>12 mmHg), uas ua rau tsim thiab rupture ntawm esophageal thiab gastric varices, ua rau mob hnyav los ntshav nrog tus neeg tuag txog li 20% -30%. AVP, raws li thawj - kab tshuaj rau kev kho tus kab mob no, muaj qhov tseeb thiab ntau lub hom phiaj
synergistic hemostatic mechanism
Visceral hematal constriction: AVP activates V1a receptor rau ntawm daim nyias nyias ntawm hematal du leeg hlwb, ua rau G protein ua ke qhia txoj hauv kev, activates phospholipase C (PLC), txhawb kev tsim thiab tso cov calcium ions los ntawm endoplasmic reticulum calcium pas dej los ntawm inositol triphosphate (KC) thiab IP activates diacylglycerol (DAG), thaum kawg ua rau myosin teeb saw phosphorylation thiab muaj zog contraction ntawm hematal du nqaij. Cov txheej txheem no nyiam ua rau visceral sanguis hlab ntsha (xws li splenic artery thiab superior mesenteric artery), txo visceral sanguis ntws los ntawm 30% -50% thiab portal vein presure los ntawm 15% -25%, yog li txo qhov cuam tshuam ntawm sanguis ntws hauv varicose leeg thiab txo qis.
Hemodynamic optimization: AVP daim ntawv cog lus peripheral sanguis hlab ntsha, ua rau kom muaj zog arterial presure (MAP), tsub kom lub plawv tom qab load, thiab indirectly txo portal vein sanguis flow. Nyob rau tib lub sijhawm, nws cov nyhuv vasoconstrictive tuaj yeem txo lub raum sanguis ntws, qhib lub renin angiotensin aldosterone system (RAAS), ntxiv txhawb kev tuav dej thiab sodium, tswj lub ntim zoo sanguis, thiab zam kom tsis txhob muaj qhov nce siab ntawm portal vein siab los ntawm qhov ntim qis sanguis.
Kev ua tau zoo ntawm kev kho mob: Ntau qhov kev sim ntsuas randomized (RCTs) tau lees paub tias AVP ua ke nrog kev kho mob endoscopic (xws li ligation thiab sclerotherapy txhaj) tuaj yeem txhim kho hemostasis ua tau zoo (los ntawm 60% mus rau 85%), txo cov ntshav rov qab (los ntawm 40% mus rau 20%), thiab txo qhov kev xav tau ntawm kev hloov pauv. Nws muaj qhov pib ua haujlwm sai (constricting sanguis hlab ntsha nyob rau hauv 5-10 feeb) thiab ntev-ntev (ntev 4-6 teev), tshwj xeeb tshaj yog haum rau txwv tsis pub los ntshav loj heev los yog hloov hemostasis ua ntej endoscopic kho.
Attention: AVP may cause side effects such as myocardial ischemia and intestinal ischemia. It is necessary to strictly monitor sanguis presure, heart rate, and lactate levels, and avoid high doses (>0.4 U / min) los yog siv ntev.
Lwm yam kev ntsuas los ntshav
AVP exerts hemostatic los ntawm ntau yam mechanisms nyob rau hauv cov kab mob nrog lub sij hawm ntev los ntshav los ntawm hereditary hemorrhagic telangiectasia (HHT), uremia, cirrhosis, thiab lwm yam.
Txhim kho platelet kev ua haujlwm: AVP ua kom phospholipase A2 (PLA2) ntawm platelet membrane los ntawm V1a receptors, txhawb nqa arachidonic acid metabolism thiab tsim thromboxane A2 (TXA2), uas yog lub zog inducer ntawm platelet aggregation. Nyob rau tib lub sijhawm, AVP tuaj yeem ua kom cov calcium ions ntau ntxiv hauv cov platelets, txhawb kev sib cuam tshuam ntawm myosin, txhim kho platelet deformation thiab tso tawm cov lus teb, thiab txo lub sijhawm los ntshav.
Txhawb kev ua haujlwm ntawm coagulation factor VIII: AVP tswj endothelial cell muaj nuj nqi thiab txhawb kev tso tawm ntawm von Willebrand factor (vWF). Raws li tus neeg nqa khoom ntawm coagulation yam VIII, vWF tuaj yeem txhim kho nws txoj kev ruaj ntseg thiab kev ua haujlwm. Tsis tas li ntawd, AVP tuaj yeem cuam tshuam ncaj qha rau thrombin ntau lawm thiab ua kom cov fibrin tsim los ntawm kev ua kom lub sijhawm tiv tauj (xws li FXII) hauv cov tshuaj tiv thaiv coagulation cascade.
Daim ntawv thov kev kho mob:
HHT: AVP tuaj yeem txo qhov zaus thiab qhov hnyav ntawm qhov ntswg, thiab txhim kho cov neeg mob lub neej zoo.
Uremia: Cov neeg mob Uremic nquag los ntshav vim qhov txawv txav ntawm platelet muaj nuj nqi thiab tsis muaj coagulation yam. AVP ua ke nrog erythropoietin (EPO) tuaj yeem kho cov ntshav ntshav thiab txhim kho hemostatic muaj nuj nqi.
Cirrhosis: Ntxiv nrog rau portal hypertension los ntshav, cov neeg mob cirrhosis feem ntau muaj coagulation tsis ua haujlwm. AVP tuaj yeem txo qhov kev pheej hmoo los ntshav tom qab phais lossis cov txheej txheem cuam tshuam los ntawm ntau txoj hauv kev ntawm hemostasis.
Kev noj tshuaj thiab kev saib xyuas: AVP feem ntau yog muab tso rau hauv cov koob tshuaj tsawg (0.01-0.04 U / min) thiab yuav tsum tau saib xyuas cov platelet suav, lub sijhawm prothrombin (PT), thiab qhib lub sijhawm thromboplastin ib nrab (APTT) kom tsis txhob muaj kev pheej hmoo ntawm thrombosis.
Central paj hlwb kev cai
Kev tswj hwm intracranial
Cov kab mob tseem ceeb ntawm cov kab mob siab intracranial siab (xws li mob hlwb raug mob, mob qog nqaij hlav hlwb, cerebral hemorrhage) yog qhov nce hauv cov ntsiab lus intracranial, uas ua rau muaj kev nce hauv intracranial siab (ICP), ua rau cerebral herniation thiab txawm tuag. AVP zoo txo ICP los ntawm cov txheej txheem hauv qab no:
Cerebral vasoconstriction: AVP activates V1a receptor ntawm cerebral hematal du nqaij, ua rau vasoconstriction los ntawm calcium dependent signaling pathway, txo cerebral sanguis flow (CBF) los ntawm 10% -20%, yog li txo cov paj hlwb thiab ICP.
Cov kev sim tsiaj tau pom tias AVP tuaj yeem txo qhov ICP ntawm lub hlwb edema qauv nas los ntawm 30 mmHg mus rau 15 mmHg, thiab cov nyhuv kav ntev li 4-6 teev.
Sanguis hlwb barrier tiv thaiv: AVP txo qhov kev qhia ntawm hematal endothelial kev loj hlob yam (VEGF), inhibits qhov nce hauv sanguis{0}}brain barrier permeability, thiab alleviates vasogenic hlwb edema. Lub caij no,argipressin acetate hmoovanti-cov nyhuv inflammatory tuaj yeem txo cov theem ntawm cov kab mob xws li qog necrosis factor - (TNF - ) thiab interleukin-6 (IL-6), ntxiv rau kev txo qis cytotoxic hlwb edema.
Daim ntawv thov kev kho mob: AVP feem ntau yog siv thaum cov tshuaj intracranial presure txo qis xws li mannitol thiab hypertonic saline tsis zoo, lossis ua ke nrog kev kho mob. Piv txwv li, hauv cov neeg mob uas raug mob lub hlwb raug mob, AVP ua ke nrog kev kho mob hypothermia tuaj yeem txo ICP thiab txhim kho kev ua haujlwm ntawm lub paj hlwb.
Ceeb Toom: Nws yog ib qho tsim nyog yuav tsum tau ua tib zoo saib xyuas lub hlwb perfusion presure (CPP=MAP-}ICP) kom tsis txhob muaj vasoconstriction ntau dhau ua rau CPP<50 mmHg and causing cerebral ischemia.
Kev tshawb fawb txog kev ua physiological
Txhawm rau tshawb xyuas seb arginine vasopressin acetate puas muaj txiaj ntsig los txo kev ntxhov siab -induced hyperthermia, wireless telemetry thev naus laus zis tau siv los ntsuas kev hloov pauv hauv lub cev kub hauv nas, thiab cov teebmeem ntawm intraperitoneal txhaj ntawm arginine vasopressin acetate thiab arginine vasopressin acetate V1 receptor blocker} nyob rau hauv kev ntxhov siab. Cov txiaj ntsig tau pom tias kev txhaj tshuaj intraperitoneal ntawm arginine vasopressin acetate tuaj yeem txo qhov kev ntxhov siab ntau heev -induced hyperthermia hauv nas, thaum txhaj tshuaj blockers tuaj yeem ua rau cov lus teb rau kev ntxhov siab -induced hyperthermia. Qhov ntawd yog hais tias, acetate arginine vasopressin tsis tsuas yog muaj cov txiaj ntsig ntawm kev txo kev ntxhov siab-induced hyperthermia hauv nas, tab sis kuj muaj cov tshuaj endogenous muaj kev tswj tsis zoo rau kev ntxhov siab-induced hyperthermia.
Tsim kom muaj cov qauv kev tshawb fawb txog kev laus neural cell siv cov ntshav qab zib -dawb kab lis kev cai ntawm nas neuroblastoma hlwb. Kev soj ntsuam ntawm cov nyhuv ntawm arginine vasopressin acetate ntawm lub voj voog ntawm tes thiab tag nrho cov protein ntawm kev sim neuronal hlwb thaum laus siv cytometry ntws. Nws tau pom tias acetate arginine vasopressin tuaj yeem tsim cov kev hloov pauv hauv lub voj voog ntawm tes thiab tag nrho cov cell protein uas ncua kev laus ntawm tes.
Cim npe nrov: Tuam Tshoj argipressin acetate manufacturers, lwm tus neeg
