Burns R C, Wu Y, Sitzmann J V
Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD, USA.
Surgery. 1995 May;117(5):488-93. doi: 10.1016/s0039-6060(05)80246-6.
We studied hemodynamic alterations in normal and three models of portal hypertension at rest, after hemorrhage, and after resuscitation to determine the role of hepatic dysfunction in the splanchnic vascular response to hemorrhage in portal hypertension.
One noncirrhotic and two cirrhotic models of portal hypertension were produced in rabbits: partial prehepatic portal vein ligation, common bile duct ligation, and carbon tetrachloride-induced cirrhosis. Animals were subjected to isovolemic hemorrhage followed by reinfusion of shed blood. Portal, central, and aortic pressures, superior mesenteric artery blood flow, and portosystemic shunt were measured.
Histologic examination showed parenchymal damage was absent in normal and portal vein ligation, severe in common bile duct ligation, and moderate in carbon tetrachloride-induced cirrhosis. All portal hypertensive animals exhibited diminished splanchnic vasoconstrictive response to hemorrhage compared with normal. The carbon tetrachloride cirrhosis group had severe cirrhotic changes, minimal portosystemic shunt, and mildly diminished constrictive response. In contrast, the portal vein ligation and common bile duct ligation animals had larger portosystemic shunts, markedly diminished constrictive response, and less severe parenchymal damage. A direct correlation existed between magnitude of rise in portal venous pressure or degree of portosystemic shunt and the fall in mesenteric resistance or diminution of vasoconstrictive response to hemorrhage.
We concluded that the abnormal splanchnic vascular response in portal hypertension is relatively independent of the degree of hepatic parenchymal injury, but it is related to the degree of portal hypertension and possibly to splanchnic hyperemia.
我们研究了正常及三种门静脉高压模型在静息状态、出血后及复苏后的血流动力学改变，以确定肝功能障碍在门静脉高压时内脏血管对出血反应中的作用。
在兔身上建立一种非肝硬化和两种肝硬化门静脉高压模型：部分肝前门静脉结扎、胆总管结扎及四氯化碳诱导的肝硬化。动物先进行等容性出血，随后回输流出的血液。测量门静脉、中心静脉和主动脉压力、肠系膜上动脉血流量及门体分流。
组织学检查显示，正常及门静脉结扎组无实质损伤，胆总管结扎组损伤严重，四氯化碳诱导的肝硬化组损伤中度。与正常动物相比，所有门静脉高压动物对出血的内脏血管收缩反应均减弱。四氯化碳肝硬化组有严重的肝硬化改变、最小的门体分流及轻度减弱的收缩反应。相比之下，门静脉结扎和胆总管结扎动物有更大的门体分流、明显减弱的收缩反应及较轻的实质损伤。门静脉压力升高幅度或门体分流程度与肠系膜阻力下降或对出血的血管收缩反应减弱之间存在直接相关性。
我们得出结论，门静脉高压时内脏血管的异常反应相对独立于肝实质损伤程度，但与门静脉高压程度相关，可能还与内脏充血有关。
