Norman D A, Atkins J M, Seelig L L, Gomez-Sanchez C, Krejs G J
Gastroenterology. 1980 Oct;79(4):707-15.
Intestinal secretion and intercullular space dilatation can be induced in animal models by acute elevation of intravascular volume or portal pressure. We examined whether patients with increased portal venous pressure might represent a clinical counterpart to these animal models. Portal venous pressure, determined by hepatic wedge pressure measurement, was elevated to 10-55 mmHg (mean 29 mmHg) in 8 patients with chronic liver disease without diarrhea. Intestinal transport studies utilizing a steady-state perfusion technique revealed normal absorption of a plasmalike electrolyte solution. A solution dsigned to unmask intestinal secretion demonstrated no difference from control subjects in the movement of water, electrolytes, or protein into the intestional lumen. There was no correlation of absorption of secretion with hepatic wedge pressure. Jejunal biopsy revealed a significant increase in dilatation of intercellular spaces in patients compared to controls; this increase was not correlated with hepatic wedge pressure, but was significantly inversely correlated to plasma renin and aldosterone concentration. We conclude that patients with chronic liver disease and portal hypertension absorb water and electrolytes normally, but have mild morphologic alterations in the intestinal mucosa, possibly related to intravascular volume status.
在动物模型中，血管内容量或门静脉压力的急性升高可导致肠分泌和细胞间隙扩张。我们研究了门静脉压力升高的患者是否可能是这些动物模型的临床对应物。通过肝楔压测量确定，8例无腹泻的慢性肝病患者的门静脉压力升高至10 - 55 mmHg（平均29 mmHg）。利用稳态灌注技术进行的肠转运研究显示，类似血浆的电解质溶液吸收正常。一种旨在揭示肠分泌的溶液在水、电解质或蛋白质向肠腔内移动方面与对照受试者无差异。分泌的吸收与肝楔压无相关性。空肠活检显示，与对照组相比，患者的细胞间隙扩张显著增加；这种增加与肝楔压无关，但与血浆肾素和醛固酮浓度显著负相关。我们得出结论，慢性肝病和门静脉高压患者水和电解质吸收正常，但肠黏膜有轻度形态学改变，可能与血管内容量状态有关。
