Patients with liver cirrhosis exhibit a hyperdynamic circulatory state
as evidenced by tachycardia and an increase in cardiac output accompa
nied by an elevation of sympathetic tone. This condition is due to the
excessive release of nitric oxide (NO), an endogenous vasodilator, wh
ich is in turn related to the abnormal induction of NO synthase. The p
resent study investigated whether the intravenous infusion of L-argini
ne, the precursor of NO, may cause a similar hyperdynamic circulatory
state. A new method, the analysis of power spectrum heart rate variabi
lity, was used to evaluate autonomic nervous activity. Twenty patients
with liver cirrhosis underwent continuous Holter monitoring of the EC
G during the intravenous administration of L-arginine (10 g) (Fisher's
solution) infused over 60 min. Power spectral analysis was computed f
rom 512 beats of the Holter ECG data. Low frequency (LF; 0.04-0.15 Hz)
and high frequency (HF; 0.15-0.40 Hz) spectral powers and the ratio o
f LF to HF (LF/HF) were calculated every 10 min before and after the i
nfusion of L-arginine. The LF power, which reflects sympathetic tone m
odified by vagal tone, and the LF/HF, an indicator of sympathetic tone
, were both significantly increased during the infusion (p<0.05). HF p
ower, an indicator of parasympathetic tone, showed no significant chan
ge in the early stage of the infusion but was significantly increased
in the late stage (p<0.05). The administration of L-arginine thus led
to an elevation of sympathetic tone. Fisher's solution, which is admin
istered to patients with hepatic insufficiency, contains L-arginine, a
nd may also produce a hyperdynamic circulatory state as an adverse eff
ect related to an elevation of the plasma level of NO by L-arginine. T
he monitoring of such patients is thus indicated.