The effect of augmenting portal venous inflow on intrahepatic pressure andresistance in the isolated perfused porcine liver

Citation
Lr. Jiao et al., The effect of augmenting portal venous inflow on intrahepatic pressure andresistance in the isolated perfused porcine liver, HEP-GASTRO, 48(40), 2001, pp. 1011-1014
Citations number
26
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
HEPATO-GASTROENTEROLOGY
ISSN journal
01726390 → ACNP
Volume
48
Issue
40
Year of publication
2001
Pages
1011 - 1014
Database
ISI
SICI code
0172-6390(200107/08)48:40<1011:TEOAPV>2.0.ZU;2-2
Abstract
Background/Aims: The literature regarding the relationship between portal v enous flow and pressure is controversial The aim of this study was to exami ne the effects of doubling portal venous inflow on hepatic hemodynamics, Methodology: Portal venous pressure, intrahepatic portal venous resistance, hepatic arterial pressure and intrahepatic arterial resistance were assess ed during basal portal venous inflow (756 +/- 142mL/min; mean SD) and enhan ced portal venous inflow (1512 +/- 284mL/min) in an isolated perfused norma l Porcine liver model (n=6). Hepatic arterial flow was maintained constant throughout the experiments. Results: During the period of enhanced portal venous flow there was an incr ease in: portal venous pressure (from 9 +/-2 to 22 +/- 7mm Hg, P=0.0076); t he difference between portal venous and hepatic venous pressures (from 2 +/ -2 to 10 +/- 5mm Hg; P=0.0289); hepatic arterial pressure (from 84 +/-9 to 151 +/- 33mm Hg, P=0.0019); and intrahepatic arterial resistance (from 0.34 88 +/-0.0637 to 0.6387 +/-0.2020, P=0.0046). Conclusions: The increases in hepatic artery pressure and intrahepatic arte rial resistance are a result of the hepatic arterial 'buffer response', a p henomenon not previously demonstrated in vitro. The magnitude of the observ ed changes in portal venous and hepatic venous pressure leads to the conclu sion that, in the porcine liver, the intrahepatic venous resistance sites r eact by constricting to increases in portal venous inflow.