20xx年醫(yī)學(xué)專題—肝硬化-cirrhosis-of-liver-文庫吧
2024-11-14 12:03 本頁面
【正文】 十五頁。,Ammonia neurotoxicity hypothesis,The GI tract: 90% (about 4g/d) Kidney :谷氨酰胺酶和H+的作用(zu242。y242。ng) Muscle: 磷酸腺苷脫胺過程,Sources of ammonia:,第十一頁，共五十五頁。,Ammonia neurotoxicity hypothesis,結(jié)腸(ji233。ch225。ng)內(nèi)pH6，NH3大量彌散入血。 結(jié)腸內(nèi)pH6， NH3從血液轉(zhuǎn)入腸腔隨糞排泄,Sources of ammonia:,有毒性(d x236。nɡ)，可以通過血腦屏障,相對(xiāngdu236。)無毒性, 不能通過血腦屏障,pH6,pH6,NH3 + H+,NH4+,第十二頁，共五十五頁。,Ammonia neurotoxicity hypothesis,Clearance of ammonia:,NH3,鳥氨酸循環(huán)(xnhu225。n),尿素(ni224。o s249。)（肝）,谷氨酸,谷氨酰胺,NH4+,NH3,NH3,ATP,α酮戊二酸,ATP,血漿(xu232。jiāng)氨的去路,（肝、腦、腎）,（腎、腸）,（肺）,第十三頁，共五十五頁。,Ammonia neurotoxicity hypothesis,Clearance of ammonia: the urea cycle（尿素(ni224。o s249。)循環(huán)）,(鳥氨酸),(胍氨酸),(尿素(ni224。o s249。)),(精氨酸),(天冬氨酸),（精氨酸代琥珀酸）,(氨甲酰磷酸(l237。n suān)),第十四頁，共五十五頁。,Ammonia neurotoxicity hypothesis,Mechanisms of ammonia neurotoxicity:,Produce,Clearance,正常人的血氨生成與清除保持動態(tài)(d242。ngt224。i)的平衡； 正常人空腹靜脈血氨40~70μg/dl， 門靜脈200~300μg/dl。,第十五頁，共五十五頁。,Ammonia neurotoxicity hypothesis,Mechanisms of ammonia neurotoxicity:,Produce,Clearance,血氨生成(shēnɡ ch233。nɡ)過多：外源性和內(nèi)生性 血氨清除過少,第十六頁，共五十五頁。,Ammonia neurotoxicity hypothesis,Mechanisms of ammonia neurotoxicity:,Neurotoxic effects of ammonia: Alter the transit of amino acids, water, and electrolytes across the neuronal membrane. Inhibit the generation of both excitatory and inhibitory postsynaptic potentials. 氨對腦組織的毒性(d x236。nɡ)作用: 抑制丙酮酸脫氫酶→乙酰輔酶A減少→ 影響三羧酸循環(huán)； 氨的清除需要消耗α
醫(yī)療健康相關(guān)推薦
鄂ICP備17016276號-1