ABSTRACT
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 nitric 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 (NAC)
and prostacy-clin, 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.
KEY WORDS
liver failure - hemodynamics - cerebral edema - renal
