Henriksen J H, Parving H H, Christiansen L, Winkler K, Lassen N A
Scand J Clin Lab Invest. 1981 May;41(3):289-99. doi: 10.1080/00365518109092047.
Transvascular escape rate of albumin [TERalb, i.e. the fraction of the intravascular mass of albumin (IVMalb) passing to the extravascular space per unit time] was determined from the disappearance of i.v. injected radioiodinated serum albumin in anaesthetized pigs during control conditions and during regional venous congestion in the infradiaphragmatic area. Balloon catheters were placed in the portal vein (infrahepatic portal congestion) and in the inferior vena cava above (suprahepatic caval congestion) and below (infrahepatic caval congestion) the outlets of the hepatic veins. TERalb was on the average 13% IVMalb.h-1 under basal pressure conditions. TERalb rose significantly (p less than 0.01) during suprahepatic caval and infrahepatic portal congestion to an average of 29 and 19% IVMalb.h-1, respectively. TERalb was positively correlated to the portal pressure (r = 0.75, P less than 0.001). Only a minor increment in TERalb was found during infrahepatic caval congestion. The hepatic share of the increased TERalb during stasis above the hepatic veins was estimated to be threefold that of the extrahepatic splanchnic area. Our results point to filtration of protein, predominantely through the lining of the sinusoids and perisinusoidal space of the liver into the interstitial space around the portal vessels and further into the lymphatics, as the main mechanism of the previously demonstrated marked increase in TERalb in patients with portal venous hypertension due to cirrhosis of the liver.
白蛋白的跨血管逃逸率[TERalb,即单位时间内从血管内白蛋白质量(IVMalb)进入血管外间隙的比例]是根据麻醉猪在对照条件下以及膈下区域局部静脉充血期间静脉注射放射性碘化血清白蛋白的消失情况来确定的。将球囊导管分别置于门静脉(肝下门静脉充血)以及肝静脉出口上方(肝上腔静脉充血)和下方(肝下腔静脉充血)的下腔静脉中。在基础压力条件下,TERalb平均为13%IVMalb·h⁻¹。在肝上腔静脉充血和肝下门静脉充血期间,TERalb显著升高(p<0.01),分别平均升至29%IVMalb·h⁻¹和19%IVMalb·h⁻¹。TERalb与门静脉压力呈正相关(r = 0.75,P<0.001)。在肝下腔静脉充血期间,TERalb仅出现轻微升高。肝静脉上方淤血期间TERalb升高的部分中,肝脏所占比例估计是肝外内脏区域的三倍。我们的研究结果表明,蛋白质滤过主要通过肝血窦壁和肝血窦周围间隙进入门静脉周围的间质空间,进而进入淋巴管,这是先前证明的肝硬化门静脉高压患者TERalb显著升高的主要机制。