Voigt M D, Trey G, Levitt N S, Raine R, Lombard C J, Robson S C, Gordon G, Kirsch R E
Department of Medicine, University of Cape Town, South Africa.
J Hepatol. 1997 Mar;26(3):634-41. doi: 10.1016/s0168-8278(97)80430-8.
BACKGROUND/AIMS: Autonomic dysfunction is common in cirrhosis, and may be associated with increased mortality and hyperdynamic circulatory changes. Our aim was to investigate whether autonomic disturbances occur in extrahepatic portal vein thrombosis and their correlation with hemodynamic abnormalities.
Heart rate variation in response to standing, deep breathing, and Valsalva maneuver, and blood pressure response to sustained handgrip and to standing, were studied in 16 subjects with portal vein thrombosis (10 males, 30.8+/-2.8 years: mean+/-SE), 12 with cirrhosis (7 males, 52+/-2.3 years), and 10 healthy controls (7 males, 30.8+/-3.0 years). Supine resting, and 10- and 30-min standing epinephrine and norepinephrine levels were measured and results correlated with cardiac output.
Autonomic dysfunction occurred in 62% of portal vein thrombosis and 75% of cirrhosis subjects, but in no controls (p<0.02). Similarly, postural hypotension occurred in portal vein thrombosis (-10.25+/-0.65 mmHg, p=0.003) and cirrhosis (-7.42+/-0.82 mmHg, p=0.007) but not in controls. All groups had similar baseline epinephrine and norepinephrine concentrations. Epinephrine increased significantly in controls (45%, p<0.01 and 49%, p<0.02) after 10 of 30 min standing but not in the portal vein thrombosis or the cirrhotic group, and norepinephrine increased after 10 and 30 min standing in cirrhotics (128%, p<0.004 and 130%, p<0.008) and controls (129%, p<0.002 and 116%, p<0.004), but not portal vein thrombosis (34.5% and 39%, NS vs baseline). Portal vein thrombosis and cirrhosis groups had increased cardiac output (4441+/-509 and 3262+/-292) vs controls (1763+/-212 ml/min/m2, p<0.002), but there was no correlation with autonomic neuropathy or with catecholamine levels.
Autonomic dysfunction and impaired catecholamine response to orthostatic stress occur commonly in portal vein thrombosis and suggest an impairment of the autonomic reflex arc, but changes do not correlate with hemodynamic abnormalities.
背景/目的：自主神经功能障碍在肝硬化中很常见，可能与死亡率增加和高动力循环变化有关。我们的目的是研究肝外门静脉血栓形成时是否会出现自主神经紊乱及其与血流动力学异常的相关性。
对16例门静脉血栓形成患者（10例男性，30.8±2.8岁：均值±标准误）、12例肝硬化患者（7例男性，52±2.3岁）和10例健康对照者（7例男性，30.8±3.0岁）进行了研究，观察他们在站立、深呼吸和瓦尔萨尔瓦动作时的心率变化，以及持续握力和站立时的血压反应。测量了仰卧休息时、站立10分钟和30分钟时的肾上腺素和去甲肾上腺素水平，并将结果与心输出量相关联。
62%的门静脉血栓形成患者和75%的肝硬化患者出现自主神经功能障碍，而对照组无一例出现（p<0.02）。同样，门静脉血栓形成患者（-10.25±0.65 mmHg，p=0.003）和肝硬化患者（-7.42±0.82 mmHg，p=0.007）出现体位性低血压，而对照组未出现。所有组的基线肾上腺素和去甲肾上腺素浓度相似。对照组在站立10分钟和30分钟后肾上腺素显著增加（分别为45%，p<0.01和49%，p<0.02），而门静脉血栓形成组和肝硬化组未增加；肝硬化组和对照组在站立10分钟和30分钟后去甲肾上腺素增加（分别为128%，p<0.004和130%，p<0.008以及129%，p<0.002和116%，p<0.004），而门静脉血栓形成组未增加（分别为34.5%和39%，与基线相比无统计学意义）。门静脉血栓形成组和肝硬化组的心输出量高于对照组（分别为4441±509和3262±292）（对照组为1763±212 ml/min/m2，p<0.002），但与自主神经病变或儿茶酚胺水平无关。
自主神经功能障碍和儿茶酚胺对直立应激的反应受损在门静脉血栓形成中很常见，提示自主神经反射弧受损，但这些变化与血流动力学异常无关。
