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作 者:周新民[1] 许其增[1] 李石[2] 高河元[1] 陈之航[1] 刘英[1]
机构地区:[1]南京军区福州总医院 [2]上海长征医院
出 处:《解放军医学杂志》1992年第4期278-281,共4页Medical Journal of Chinese People's Liberation Army
摘 要:采用放射免疫分析法测定代偿、失代偿及肝肾综合征(HRS)三期患者尿PGE_2、TXB_2排泄值及血浆ANP、AVP浓度,发现代偿期无腹水患者上述4种血管活性物质均明显增高,随病情加重,PGE_2逐步下降,TXB_2进行性升高,血浆ANP无明显变化,AVP则进行性降低。结果提示早期肝硬变患者即有钠水代谢的紊乱,血管活性物质之间相互作用的失衡是钠水潴留加重及HRS发生发展的重要因素。Urinary excretion of prostaglandin E2. (PGE2) and thromboxane B2 (TXB2, a stable metabolite of TXA2), atrial natriuretic peptide (ANP) and arginine vasopressin (AVP) in plasma were determined with radioimmunoassay in 30 healthy normal controls (NC) and 53 cirrhotic patients without asoites (n = 18), with ascites (n = 25) and with hepatorenal syndrome (HRS, n=10). All of four vasoactive substances in the group of cirrhotic patients without ascites were significantly higher than that in NG (P<0.05~0.001). With the worsening of cirrhosis, the excretion of PGE2 decreased while the excretion of TXB2 increased progressively; plasma ANP level showed no change, but plasma AVP level decreased markly even to normal. These data indicate that the derangement of renal hemodynamics and sodium-water homeostasis are present before ascites formation in cirrhosis, and the imbalance of four vasoactive substances is an important factor in enhancing sodium-water retention and development of HRS.
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