Saijyo T, Nomura M, Nakaya Y, Saito K, Ito S
Second Department of Internal Medicine, School of Medicine, University of Tokushima, Japan.
Liver. 1998 Feb;18(1):27-31. doi: 10.1111/j.1600-0676.1998.tb00123.x.
Patients with liver cirrhosis exhibit a hyperdynamic circulatory state as evidenced by tachycardia and an increase in cardiac output accompanied by an elevation of sympathetic tone. This condition is due to the excessive release of nitric oxide (NO), an endogenous vasodilator, which is in turn related to the abnormal induction of NO synthase. The present study investigated whether the intravenous infusion of L-arginine, the precursor of NO, may cause a similar hyperdynamic circulatory state. A new method, the analysis of power spectrum heart rate variability, was used to evaluate autonomic nervous activity. Twenty patients with liver cirrhosis underwent continuous Holter monitoring of the ECG during the intravenous administration of L-arginine (10 g) (Fisher's solution) infused over 60 min. Power spectral analysis was computed from 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 of LF to HF (LF/HF) were calculated every 10 min before and after the infusion of L-arginine. The LF power, which reflects sympathetic tone modified by vagal tone, and the LF/HF, an indicator of sympathetic tone, were both significantly increased during the infusion (p<0.05). HF power, an indicator of parasympathetic tone, showed no significant change 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 administered to patients with hepatic insufficiency, contains L-arginine, and may also produce a hyperdynamic circulatory state as an adverse effect related to an elevation of the plasma level of NO by L-arginine. The monitoring of such patients is thus indicated.
肝硬化患者表现出高动力循环状态，表现为心动过速和心输出量增加，同时伴有交感神经张力升高。这种情况是由于内源性血管舒张剂一氧化氮（NO）的过度释放所致，而这又与NO合酶的异常诱导有关。本研究调查了静脉输注NO的前体L-精氨酸是否会导致类似的高动力循环状态。采用一种新的方法——功率谱心率变异性分析，来评估自主神经活动。20例肝硬化患者在静脉输注L-精氨酸（10 g）（Fisher溶液）60分钟期间，接受了连续的动态心电图监测。从动态心电图数据的512次心跳中计算功率谱分析。在输注L-精氨酸前后，每隔10分钟计算低频（LF；0.04 - 0.15 Hz）和高频（HF；0.15 - 0.40 Hz）谱功率以及LF与HF的比值（LF/HF）。反映受迷走神经张力调节的交感神经张力的LF功率以及作为交感神经张力指标的LF/HF，在输注期间均显著增加（p<0.05）。作为副交感神经张力指标的HF功率，在输注早期无显著变化，但在后期显著增加（p<0.05）。因此，L-精氨酸的给药导致了交感神经张力升高。用于肝功能不全患者的Fisher溶液含有L-精氨酸，也可能产生高动力循环状态，作为与L-精氨酸使血浆NO水平升高相关的不良反应。因此，对这类患者进行监测是必要的。
