Lindgren S, Lilja B, Verbaan H, Sundkvist G
Gastroenterology-Hepatology Division, University of Lund, University Hospital of Malmö, Sweden.
Scand J Gastroenterol. 1996 Nov;31(11):1120-4. doi: 10.3109/00365529609036897.
Advanced chronic liver disease is characterized by peripheral arterial vasodilation and increased plasma catecholamine concentrations. These haemodynamic alterations may reflect impaired vascular responsiveness due to autonomic nerve dysfunction.
Three established non-invasive tests based on the heart reactions to deep breathing (expiratory/inspiratory (E/I) ratio) and to tilt (acceleration and brake indices) were used to evaluate age-related autonomic nerve function in 27 patients with chronic alcoholic and non-alcoholic liver disease. Liver function was estimated by demethylating capacity. The results were compared with a control group consisting of 56 healthy individuals.
Overall, 12 patients (52%) had autonomic neuropathy (10 of 13 (77%) patients with alcoholic and 2 of 14 (14%) with non-alcoholic liver disease). Variance analysis showed that the age-corrected E/I ratio, but not the acceleration and brake indices, was significantly decreased compared with controls both in patients with alcoholic and non-alcoholic liver disease, indicating vagal nerve dysfunction (P < 0.0001 and 0.0133, respectively). The decrease in E/I ratio was also significantly more pronounced (-1.77 (0.62) (median (interquartile range)) versus 0.76 (0.70); P = 0.049) in patients with alcoholic compared with non-alcoholic liver disease. Furthermore, in contrast to non-alcoholics, patients with alcoholic liver disease were unable to increase their diastolic blood pressure after return to upright from a tilted position, indicating additional sympathetic neuropathy.
Autonomic, mainly vagal, nerve dysfunction is common in patients with liver diseases and is further exaggerated by alcohol abuse. Autonomic neuropathy may contribute to altered vascular responsiveness in patients with chronic liver diseases.
晚期慢性肝病的特征是外周动脉血管舒张和血浆儿茶酚胺浓度升高。这些血流动力学改变可能反映了自主神经功能障碍导致的血管反应性受损。
采用三种基于心脏对深呼吸(呼气/吸气(E/I)比值)和倾斜(加速度和制动指数)反应的成熟非侵入性测试,评估27例慢性酒精性和非酒精性肝病患者的年龄相关自主神经功能。通过去甲基化能力评估肝功能。将结果与由56名健康个体组成的对照组进行比较。
总体而言,12例患者(52%)存在自主神经病变(13例酒精性肝病患者中的10例(77%)和14例非酒精性肝病患者中的2例(14%))。方差分析显示,与对照组相比,酒精性和非酒精性肝病患者经年龄校正的E/I比值均显著降低,但加速度和制动指数未降低,表明迷走神经功能障碍(分别为P < 0.0001和0.0133)。与非酒精性肝病患者相比,酒精性肝病患者的E/I比值下降也更为明显(中位数(四分位间距)为-1.77(0.62)对0.76(0.70);P = 0.049)。此外,与非酒精性肝病患者不同,酒精性肝病患者从倾斜位置恢复直立后无法提高舒张压,表明存在额外的交感神经病变。
自主神经功能障碍,主要是迷走神经功能障碍,在肝病患者中很常见,并且因酒精滥用而进一步加重。自主神经病变可能导致慢性肝病患者血管反应性改变。