Kev txhaj tshuaj Argipressin

Central ntshav qab zib insipidus yog ib yam kab mob uas tshwm sim los ntawm polyuria, nqhis dej, tsis tshua muaj qhov nqus zis, thiab cov zis hypotonic, tshwm sim los ntawm kev sib xyaw tsis txaus, tso tawm, lossis tso tawm ntawm cov tshuaj tiv thaiv kab mob (AVP) vim hypothalamic pituitary lesions. AVP, raws li cov tshuaj tseem ceeb rau kev kho mob hauv nruab nrab ntshav qab zib insipidus, muaj cov txheej txheem ntawm kev ua haujlwm zoo: nws tshwj xeeb khi rau V2 receptor ntawm lub raum ntawm lub raum khaws cov hlab ntsha epithelial hlwb, ua kom lub cev intracellular adenylate cyclase (AC), txhawb nqa qib siab ntawm cyclic adenosine monophosphate thiab triglycerides ntawm protein AMP. (PKA). PKA phosphorylates ib tug series ntawm downstream lub hom phiaj proteins, thaum kawg upregulating cov lus qhia ntawm aquaporin-2 (AQP2) thiab txhawb nqa nws kev thauj mus los ntawm intracellular vesicles mus rau lub luminal daim nyias nyias, tsim ua hauj lwm dej raws.

Cov txheej txheem no tseem ceeb txhim kho cov permeability ntawm lub raum khaws cov ducts rau dej, zoo heev txhim kho kev ua haujlwm ntawm dej reabsorption. Yog li ntawd, cov zis tso zis yog txo los ntawm 50% -80%, thiab cov zis osmotic siab tuaj yeem rov qab los ntawm lub xeev osmotic qis (<300 mOsm/kg H ₂ O) to near normal levels (600-1200 mOsm/kg H ₂ O). In clinical practice, alternative treatment of AVP can significantly improve patient symptoms: reducing the frequency of polyuria from tens of times a day to several times a day, significantly alleviating irritability and thirst, significantly improving nighttime sleep quality, and fundamentally improving quality of life. Long term use requires regular monitoring of blood sodium, urine osmotic pressure and other indicators to avoid water retention or hypernatremia and other complications.

Nocturnal enuresis yog ib qho kev loj hlob tsis zoo hauv cov menyuam yaus, uas yog hais txog kev tso zis ntawm cov menyuam yaus hnub nyoog qis dua 5 xyoos thaum pw tsaug zog, tshwm sim tsawg kawg ob zaug hauv ib lub lis piam thiab kav ntev dua 3 lub hlis. Nws cov kab mob cuam tshuam nrog ntau yam xws li kev tso tawm tsis txaus ntawm cov tshuaj tua kab mob thaum hmo ntuj, txo lub zais zis, thiab pw tsaug zog tsis zoo. AVP tau dhau los ua ib txoj hauv kev tseem ceeb rau kev kho mob nocturnal enuresis los ntawm kev ntxiv cov physiological secretion deficiency ntawm antidiuretic hormone thaum hmo ntuj. Kev tshawb fawb tau pom tias kev tswj hwm qhov ncauj ntawm AVP analogs (xws li desmopressin) ua ntej pw hauv cov menyuam yaus hnub nyoog 6 thiab siab dua tuaj yeem txo cov zis thaum hmo ntuj, ua kom lub sijhawm tso zis thawj zaug, thiab txo qhov zaus ntawm enuresis.

Nws cov txheej txheem ntawm kev txiav txim suav nrog: ncaj qha txhim kho cov reabsorption ntawm cov dej los ntawm lub raum khaws cov duct thiab txo cov zis thaum hmo ntuj; Los ntawm kev kho qhov pib ntawm qhov pib ntawm lub paj hlwb hauv nruab nrab, cov me nyuam txoj kev nkag siab ntawm lub zais zis tuaj yeem txhim kho, yog li txhawb kev tswj hwm tus kheej thiab tso zis thaum pw tsaug zog. Hauv kev siv tshuaj kho mob, AVP, raws li kev siv tshuaj tsis yog tshuaj, feem ntau yog siv los ua ke nrog kev coj tus cwj pwm (xws li kev tso zis tso quav thiab zais zis), nrog rau tag nrho cov txiaj ntsig zoo ntawm 60% -80%, thiab cov kev mob me me (xws li mob taub hau thiab qhov ntswg congestion), thiab ua raws li cov neeg mob siab.

Septic shock yog ib qho mob hnyav uas tshwm sim los ntawm cov kab mob inflammatory teb (SIRS) tshwm sim los ntawm kev kis kab mob,argipressin txhaj tshuajCov txheej txheem tseem ceeb ntawm pathophysiological yog vasodilatory hypotension, cov ntaub so ntswg hypoperfusion, thiab cellular hypoxia. AVP activates V1a receptor nyob rau hauv daim nyias nyias ntawm vascular du leeg hlwb, ua rau G protein ua ke cov teeb liab txoj kev, ua rau lub activation ntawm phospholipase C (PLC), uas nyob rau hauv lem generates inositol triphosphate (IPv3) thiab diacylglycerol (DAG). IP v3 txhawb kev tso tawm calcium ions los ntawm lub pas dej endoplasmic reticulum calcium, thaum DAG activates protein kinase C (PKC). Cov nyhuv synergistic ntawm ob ua rau nce intracellular calcium ion concentration, ua rau myosin teeb saw phosphorylation thiab thaum kawg ua rau vascular du nqaij contraction.

Cov txheej txheem no ua rau AVP yog cov tshuaj tseem ceeb rau kev kho mob septic shock:

Boosting effect: AVP tuaj yeem ua rau muaj kev nce siab hauv lub siab (MAP) thiab txhim kho cov ntaub so ntswg perfusion. Cov koob tshuaj tsawg (0.01-0.04 U / min) tuaj yeem ua rau lub raum cov hlab ntsha thiab txo cov ntshav raum; Cov koob tshuaj siab (0.1-0.4 U / min) tuaj yeem ua rau lub cev vasoconstriction thiab nce MAP los ntawm 20% -30%.
Synergistic effect: Thaum ua ke nrog cov tshuaj catecholamine (xws li norepinephrine), AVP tuaj yeem txhim kho vascular rhiab heev rau catecholamines, txo lawv cov koob tshuaj, thiab yog li txo qhov kev pheej hmoo ntawm kev phiv xws li arrhythmia thiab myocardial ischemia.
Kev txhim kho ntawm cov ciaj sia taus: Ntau qhov kev sim ntsuas randomized (RCTs) tau lees paub tias kev sib xyaw ntawm AVP thiab norepinephrine hauv kev kho mob septic shock tuaj yeem txo 28 hnub kev tuag los ntawm 10% -15%, tshwj xeeb tshaj yog rau cov neeg mob uas tsis zoo rau cov lus teb yooj yim catecholamines.

Cardiopulmonary resuscitation yog ib qho kev kho mob xwm txheej ceev rau cov neeg mob uas muaj lub plawv nres, thiab nws txoj kev vam meej yog nyob ntawm kev kho mob sai sai ntawm cov hlab ntshav siab (CPP) thiab myocardial oxygen mov. Nyob rau hauv lub plawv nres nyob rau hauv uas tsis yog shockable rhythms xws li ventricular ntes thiab avascular hluav taws xob kev ua si, ib txwm adrenaline kev kho mob tej zaum yuav muaj kev txwv tsis pub siv vim desensitization ntawm beta receptors los yog nce myocardial oxygen noj.

AVP optimizes CPR hemodynamics los ntawm cov txheej txheem hauv qab no:

Lwm txoj kev adrenaline: AVP (40 U) tuaj yeem hloov qhov koob thib ib lossis thib ob ntawm adrenaline, thiab nws cov nyhuv vasoconstrictive tsis nyob ntawm beta adrenergic receptors, zam kev pheej hmoo ntawm arrhythmia uas adrenaline yuav ua rau.
Txhim kho CPP: AVP nce CPP nce ntxiv (los ntawm<10 mmHg to>20 mmHg) thiab txhawb nqa myocardial ntshav khiav rov qab los ntawm kev nruj nruj cov hlab ntsha peripheral, txo cov ntshav rov qab ntim, thiab nce intrathoracic siab.
Improving long-term prognosis: Animal experiments and clinical studies have shown that AVP combined with adrenaline can increase the rate of spontaneous circulation recovery (ROSC) by 15% -20%, especially for patients with long-term ischemia (>10 feeb) lossis qis -kub plawv nres.

Vasodilatory hypotension yog ib qho teeb meem tshwm sim hauv cov txheej txheem kho mob xws li tshuaj loog thiab cardiopulmonary bypass (CPB), uas yog tshwm sim los ntawm kev txo qis hauv vascular du leeg ua rau txo qis hauv peripheral tsis kam. AVP, dhau los ntawm nws cov V1a receptor-kev kho mob vasoconstriction, tau dhau los ua kev kho mob zoo rau hom hypotension.

Hypotension tom qab tshuaj loog: Hauv kev siv tshuaj loog lossis tshuaj loog, AVP (0.01-0.04 U / min) tuaj yeem kho hypotension sai, txo qis kev vam khom ntawm cov kua dej resuscitation lossis cov tshuaj vasoactive, thiab zam kev pheej hmoo ntawm ntim ntau dhau.

Cov tawv nqaij hypotension tom qab CPB: Thaum lub sij hawm CPB, kev sib cuag ntawm cov ntshav thiab cov khoom siv dag zog activates inflammatory reactions, ua rau poob ntawm vascular tone. AVP cog lus rau cov hlab ntsha, nce MAP, txo kev siv cov tshuaj inotropic zoo xws li dopamine thiab dobutamine, thiab txo qis myocardial oxygen noj thiab kev pheej hmoo ntawm arrhythmia.
Daim ntawv thov pej xeem tshwj xeeb: Rau cov neeg laus lossis cov neeg muaj lub raum tsis txaus, AVP muaj txiaj ntsig zoo dua vasoconstrictive vimargipressin txhaj tshuajtsis tso siab rau renin-angiotensin system, zam kev pheej hmoo ntawm kev cuam tshuam ntawm angiotensin converting enzyme inhibitors (ACEIs) lossis angiotensin receptor antagonists (ARBs).