McLaren M, Braye S, Fleming J, Karran S, Taylor I
Gut. 1987 Jun;28(6):663-7. doi: 10.1136/gut.28.6.663.
An experimental model of cirrhosis was developed in the rat to assess the effect of disease and pharmacological manipulation on blood flow, shunting and portal pressure. With progression in the severity of histological cirrhosis there was a steady fall in effective liver blood flow as measured with radioisotope labelled colloid. This corresponded to a rise in portal pressure and shunting with a close correlation between the two (r = 0.7, p less than 0.01). In control animals and when portal hypertension was caused by extrahepatic obstruction, beta-blockade with propranolol, but not selective beta 2 blockade, significantly decreased liver blood flow. With cirrhosis there was a variable response to propranolol depending on the histological severity of disease, the height of portal pressure and degree of shunting. There is a possibility therefore that a potential may exist for lowering portal pressure by manipulating intrahepatic shunting.
在大鼠中建立了肝硬化实验模型,以评估疾病和药物干预对血流、分流和门静脉压力的影响。随着组织学肝硬化严重程度的进展,用放射性同位素标记胶体测量的有效肝血流量稳步下降。这与门静脉压力升高和分流增加相对应,两者之间密切相关(r = 0.7,p < 0.01)。在对照动物以及由肝外梗阻引起门静脉高压时,普萘洛尔进行β受体阻滞,但选择性β2受体阻滞则不然,会显著降低肝血流量。对于肝硬化,根据疾病的组织学严重程度、门静脉压力高度和分流程度,对普萘洛尔有不同的反应。因此,通过操纵肝内分流来降低门静脉压力存在可能性。