Circulatory, respiratory, cerebral, and renal derangements in acute liver failure: Pathophysiology and management

被引:108
作者
Ellis, A [1 ]
Wendon, J [1 ]
机构
[1] UNIV LONDON KINGS COLL,SCH MED & DENT,LONDON WC2R 2LS,ENGLAND
关键词
liver failure; hemodynamics; cerebral edema; renal;
D O I
10.1055/s-2007-1007251
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Many of the hemodynamic abnormalities seen in acute liver failure (ALF) have now been characterized. A lowered systemic vascular resistance with a raised cardiac output are prominent features, which in part are modulated by niti ic oxide (NO). At a cellular level, oxygen supply and utilization are impaired by changes in vascular tone, plugging of nutritive vessels, and pathological shunting. The use of N-acetylcysteine (NAG) and prostacyclin, a vasodilator, have been shown to increase oxygen utilization in the microcirculation. NAC may act by enhancing the effect of NO on guanylate cyclase, increasing the formation of cyclic 3',5'-guanosine monophosphate (cGMP), and thereby resulting in vasodilatation. This suggests that despite overproduction of NO in ALF, there is a shortage/failure of utilization at a cellular level. Appropriate management of these patients should be based on a good knowledge of the underlying pathophysiology, and thus on monitoring, during the course of the disease.
引用
收藏
页码:379 / 388
页数:10
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