Angiotensin II Acetate

Shaanxi BLOOM Tech Co., Ltd. yog ib qho ntawm cov tuam ntxhab thiab cov muag khoom ntawm angiotensin ii acetate hauv Suav teb. Txais tos rau cov lag luam wholesale bulk zoo angiotensin ii acetate muag ntawm no los ntawm peb lub hoobkas. Kev pabcuam zoo thiab tus nqi tsim nyog muaj.

Angiotensin II acetate(CAS: 58-49-1) yog cov tshuaj ntsev ua ke los ntawm kev sib txuas ntawm angiotensin II (Ang II) nrog acetate radicals. Nws cov qauv molecular yog ua raws li cov active peptide ib ntus DRVYIHPF, thiab cov ntsev acetate no khaws tag nrho cov kev ua ub no ntawm cov niam txiv peptide. Chemically, cov khoom zoo li ib tug dawb los yog tawm-dawb crystalline hmoov. Nws nta cov dej solubility zoo heev, uas ua kom yooj yim rau kev npaj cov kua tshuaj formulations. Nyob rau hauv cov nqe lus ntawm stability, no acetate outperforms tus thawj DRVYIHPF peptide. Nws tswj cov qauv molecular ruaj khov thiab muaj zog lom nyob rau hauv cov txheej txheem kaw, txias thiab qhuav cia, thiab tsis tshua muaj kev cuam tshuam los ntawm kev hloov pauv kub thiab hloov pH me ntsis. Ua tsaug rau optimized physicochemical zog, nws kuj muab ntau dua bioavailability tom qab kev tswj hwm.

 

Cov qauv tshuaj

Angiotensin II acetate(C50H71N13O10) yog ntsev compound ntawm DRVYIHPF. Nws yog ib qho nquag peptide tsim los ntawm 8 amino acids, nrog rau cov tshuaj formula C50H71N13O10. Nws muaj zog physiological kev ua si thiab koom nyob rau hauv ib tug series ntawm cov txheej txheem tseem ceeb xws li kev tswj ntshav siab thiab kua dej tshuav nyiaj li cas hauv lub cev. Acetate yog tsim los ntawm acetylation cov tshuaj tiv thaiv ntawm qee cov amino pawg hauv DRVYIHPF molecules, uas txhim kho cov solubility thiab stability ntawm cov tshuaj.Piv txwv li tus thawj DRVYIHPF, daim ntawv acetate ntawm DRVYIHPF muaj kev ruaj ntseg zoo dua li cov tshuaj molecule, ua kom yooj yim rau kev tswj kev ua haujlwm hauv cov tshuaj tsis muaj degradation.

Cov yam ntxwv no ua rau nws ib txwm siv cov tshuaj hauv kev kho mob hnyav, tshwj xeeb tshaj yog tsim rau kev txhaj tshuaj thiab intravenous infusion.Clinically, tus neeg sawv cev no feem ntau siv los tswj cov ntshav siab. Nws ua hauj lwm pab raws li ib tug txhim khu kev qha kev xaiv kho mob rau cov mob tseem ceeb xws li mob circulatory tsis ua hauj lwm thiab ntau yam kev poob siab, muaj qhov tseem ceeb ntawm kev kho mob. Piv nrog cov ntshiab DRVYIHPF, acetate ntsev boasts superior stability, solubility thiab bioavailability. Cov txiaj ntsig zoo no ua rau nws muaj kev nyab xeeb dua thiab ua tau zoo dua rau kev siv tshuaj txhaj tshuaj, thiab nws tau dhau los ua ib qho kev nyiam hauv kev kho mob xwm txheej ceev thiab kev kho mob tseem ceeb.

Pharmacological yam ntxwv

 

Acetate, zoo li DRVYIHPF, tawm tsam lawv lub cev thiab tshuaj tshuaj los ntawm kev khi rau DRVYIHPF receptor type 1 (AT1 receptor) thiab hom 2 (AT2 receptor). AT1 receptor yog lub hom phiaj tseem ceeb ntawm DRVYIHPF, suav nrog cov kev taw qhia xws li vasoconstriction, aldosterone secretion, sympathetic nervous system excitation, cell proliferation, thiab fibrosis.

 

Acetate, vim nws cov tshuaj lom neeg ruaj khov thiab kev ua haujlwm lom neeg, yog siv dav hauv kev kho mob ntawm cov neeg mob hnyav, tshwj xeeb tshaj yog thaum muaj kev poob siab, mob ntshav siab, thiab lwm yam, txhawm rau txhim kho hemodynamic stability los ntawm kev nce ntshav siab hauv lub sijhawm luv luv. Piv nrog rau kev txhaj tshuaj ncaj qha ntawm thawj daim ntawv ntawm DRVYIHPF, daim ntawv acetate muaj kev ruaj ntseg zoo dua hauv kev daws teeb meem, uas yuav pab txo qis cov tshuaj tsis paub meej thiab muaj kev pheej hmoo ntawm kev siv tshuaj.

DRVYIHPF, abbreviated li DRVYIHPF, yog ib qho tshuaj siv dav hauv kev kho mob. Nws yog ib qho tseem ceeb ntawm cov tshuaj hormones hauv renin angiotensin aldosterone system (RAAS), muaj kev koom tes hauv kev tswj hwm cov txheej txheem tseem ceeb xws li ntshav siab, kua dej sib npaug, thiab vasoconstriction. Zoo ib yam li cov txheej txheem ntawm kev txiav txim ntawm DRVYIHPF, nws tsuas yog txhawb nqa AT1 thiab AT2 receptors los ua kom lub cev muaj zog ntawm lub cev xws li cov hlab ntsha, lub plawv, thiab ob lub raum, yog li kho tau zoo xws li hypotension thiab poob siab.Los ntawm kev ua haujlwm ntawm AT1 receptor, G protein txuas txuas receptor signaling txoj hauv kev ua kom muaj calcium ntau ntxiv, contraction ntawm vascular smooth nqaij.

1. Siv rau kev kho mob ntawm tus mob hypotension thiab poob siab

Ib qho ntawm cov kev kho mob tseem ceeb ntawmangiotensin II acetateyog nyob rau hauv kev kho mob ntawm mob hypotension thiab poob siab. Kev poob siab yog ib qho kev kho mob xwm txheej ceev uas cuam tshuam nrog kev tsis txaus thiab kev tso ntshav ntawm cov ntshav, ua rau cov pa oxygen tsis txaus rau cov ntaub so ntswg thiab lub cev. Muaj ntau hom kev poob siab, nrog rau kev poob siab septic, kev poob siab, tsis tshua muaj suab nrov, thiab lwm yam, thiab feem ntau ntawm cov hom no tau nrog vasodilation, ua rau cov ntshav siab poob qis.
Nyob rau hauv cov ntaub ntawv no, nws muaj zog vasoconstrictive nyhuv yuav pab kom tus neeg mob cov ntshav siab sai.

 

Li no ua rau peripheral vascular tsis kam thiab nce ntshav siab. Tsis tas li ntawd, DRVYIHPF tuaj yeem pab ua kom cov kua dej sib npaug los ntawm kev txhawb nqa lub zais ntawm aldosterone thiab txhim kho sodium reabsorption.

Daim ntawv thov ib txwm: Cov neeg mob uas muaj ntau lub cev tsis ua haujlwm
Hauv cov neeg mob uas muaj ntau lub cev tsis ua haujlwm (MODS), tshwj xeeb tshaj yog cov neeg muaj kab mob hnyav lossis raug mob, cov ntshav ntim yooj yim ntxiv feem ntau tsis tuaj yeem kho cov ntshav txaus perfusion vim qhov pheej muaj vasodilation thiab hypotension. Hauv qhov no, kev siv tuaj yeem kho hypotension sai thiab txhim kho lub cev perfusion, zam kev puas tsuaj los ntawm lub cev hypoxia.

2. Kev siv rau hauv cov kab mob raum

Nws daim ntawv thov tsis txwv rau kev kho mob hypotension, tab sis kuj ua lub luag haujlwm tseem ceeb hauv kev tswj cov kab mob raum. Lub sij hawm ntev hypotension los yog hypoperfusion tuaj yeem ua rau lub raum tsis ua haujlwm, thiab hauv cov xwm txheej hnyav, yuav ua rau muaj kev puas tsuaj rau lub raum tsis ua haujlwm. Los ntawm kev siv nws cov txiaj ntsig vasoconstrictive, nws tuaj yeem ua rau muaj zog perfusion ntawm ob lub raum thiab tswj cov glomerular filtration rate (GFR).
Hauv qee cov neeg mob uas muaj kab mob raum ntev, tshwj xeeb tshaj yog cov neeg uas muaj lub siab xav mus rau cov ntshav siab qis, siv nws tuaj yeem pab txhim kho lub raum ua haujlwm thiab tiv thaiv kev tsis zoo ntxiv.

3. Adjuvant kev kho mob rau cov kab mob plawv

Nws kuj tau siv rau hauv kev tswj mob hnyav ntawm cov kab mob plawv. Piv txwv li, nyob rau hauv cov neeg mob uas mob plawv tsis ua hauj lwm, ua kom lub preload thiab afterload ntawm lub plawv los ntawm vasoconstriction tuaj yeem pab ua kom cov teebmeem hemodynamic ntawm lub plawv thiab txhim kho nws cov dej ntws.
Hauv cov txheej txheem kev kho mob ntawm kev rov pib lub plawv tom qab lub plawv nres, raws li cov tshuaj vasopressor, nws tuaj yeem ua rau cov ntshav siab, ua kom lub cev muaj zog xws li lub plawv thiab lub hlwb, thiab txo cov teeb meem tom qab cardiopulmonary resuscitation.

4. Ua ke siv nrog lwm yam tshuaj

Nws yog feem ntau siv ua ke nrog lwm cov tshuaj, tshwj xeeb tshaj yog nyob rau hauv kev kho mob ntawm cov neeg mob hnyav, thiab feem ntau yog siv ua ke nrog vasopressors xws li norepinephrine thiab dopamine kom ua tiav kev txhawb nqa hemodynamic. Qhov kev sib xyaw ua ke no tuaj yeem ua rau kom rov zoo ntawm cov ntshav siab thiab tswj cov ntshav ntws hauv ntau lub cev, tshwj xeeb tshaj yog nyob rau hauv cov kabmob xws li lub plawv, hlwb, thiab ob lub raum uas xav tau cov ntshav siab.

Cov txheej txheem tseem ceeb tau siv hauv kev kho mob yog nws cov txiaj ntsig kho mob rau mob hypotension thiab poob siab. Nws pab cov neeg mob hnyav rov qab los ntawm hemodynamic stability los ntawm kev nce ntshav siab, tshwj xeeb tshaj yog nyob rau hauv cov xwm txheej hauv qab no uas nws muaj cov ntawv thov tseem ceeb:

1. Mob hypotension thiab poob siab

 

Nyob rau hauv ntau hom kev poob siab, tshwj xeeb tshaj yog septic shock, hemorrhagic shock, thiab lwm yam, nws muaj zog vasoconstrictive nyhuv pab rov qab peripheral vascular tsis kam, nce ntshav siab sai, thiab kho lub cev perfusion. Qhov no yog vim kev poob siab feem ntau nrog rau loj - nplai vasodilation thiab ntshav siab poob. Los ntawm kev ncaj qha vasoconstriction, lub xeev hypotensive no tuaj yeem kho tau sai, txhim kho perfusion ntawm cov kabmob tseem ceeb.

2. Mob plawv tsis ua hauj lwm

 

Thaum ua ntawv thov rau kev tswj cov mob plawv tsis ua hauj lwm, tus neeg sawv cev no pab ntxiv dag zog rau lub plawv dhia ua haujlwm los ntawm kev nce ntshav siab thiab txhawb nqa lub plawv ua ntej. Nws ua los ntawm activating AT1 receptors, uas ua rau kom myocardial contractility thiab txhim kho venous ntshav rov qab. Yog li ntawd, tag nrho lub siab lub nra ntawm lub plawv yog zoo alleviated.

3. Hemodynamic kev them nyiaj yug rau siab - cov neeg mob uas pheej hmoo

 

Feem ntau siv rau cov neeg mob uas muaj kev pheej hmoo siab - uas xav tau kev txhawb nqa hemodynamic, xws li cov neeg mob hnyav tom qab kev phais, cov neeg mob uas muaj ntau lub cev tsis ua haujlwm, thiab lwm yam. Los ntawm kev ua kom ntshav siab sai,angiotensin II acetatetuaj yeem pab cov neeg mob no tswj cov cim tseem ceeb ruaj khov thiab tiv thaiv lub cev hypoperfusion.

Nws tau ua kom pom qhov zoo tshwj xeeb hauv cov hauv qab no:

1. Controllability ntawm ntev - lub sij hawm intravenous infusion

Vim nws txoj kev ruaj khov thiab dej solubility, cov hlab ntsha yog tsim nyog rau lub sij hawm ntev - intravenous infusion, tshwj xeeb tshaj yog thaum cov neeg mob xav tau kev tswj ntshav siab. Hauv qhov sib piv, ib txwm siv DRVYIHPF, vim nws luv luv ib nrab - lub neej, yog qhov nyuaj los tuav lub sijhawm ntev - kev ua tau zoo thiab yuav tsum tau hloov tshuaj ntau zaus.

2. Haum rau kev kho mob ntawm tus mob hypotension

Nyob rau hauv cov xwm txheej xws li mob hypotension thiab poob siab, nws tuaj yeem siv sai sai thiab tswj cov hemodynamic stability tsis tu ncua.

Qhov no yog qhov tseem ceeb tshwj xeeb tshaj yog nyob rau hauv cov mob hnyav hnyav xws li septic shock thiab hemorrhagic shock, vim nws tuaj yeem pab cov kws kho mob sai kho ntshav siab thiab xyuas kom lub cev perfusion.

3. Ntau qhov kev tswj xyuas ntau npaum li cas

Vim tias nws muaj zog ruaj khov, kev hloov kho ntau npaum li cas, thiab ntau tus neeg mob cov lus teb rau cov tshuaj, qhov no yuav pab kom tsis txhob muaj kev pheej hmoo ntawm kev kub siab ntau dhau lossis siv tshuaj tsis txaus.

1. Galletti, F., et al. (2020). * DRVYIHPFI: Lub luag haujlwm tseem ceeb ntawm kev ua haujlwm ntawm lub plawv *. Phau ntawv Journal of Hypertension, 38(5), 783-792.

2. Joffe, SP, & Singh, AK (2018). * DRVYIHPF nyob rau hauv mob circulatory shock thiab sepsis *. Phau ntawv Journal of Critical Care, 44, 153-160.

3. Fletcher, RL, et al. (2017). * Pharmacokinetics thiab pharmacodynamics ntawm DRVYIHPF hauv cov neeg mob poob siab *. Phau ntawv Journal of Clinical Pharmacology, 57(12), 1549-1557.

4. Mendoza, AS, et al. (2019). * Lub luag haujlwm ntawm DRVYIHPF hauv pathophysiology ntawm ntshav siab thiab kab mob plawv*. Phau ntawv Journal of Clinical Hypertension, 21(9), 1281-1289.

5. Giapreza, INN-angiotensin2 acetate (https://www.ema.europa.eu/en/documents/product-information/giapreza-epar- khoom-information_en.pdf)

6. AngiotensinII Acetate (https://evsexplore.semantics.cancer.gov/evsexplore/concept/ncit/C142924)

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