The relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver.
BACKGROUND
Portal hypertension is associated with gross haemodynamic disturbances characterised by high cardiac output, low peripheral vascular resistance, increased splanchnic blood flow, and portal systemic shunting.


OBJECTIVE
To study the relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver.


METHODS
Different sized microspheres were sequentially injected into the portal vein of male Wistar rats.


RESULTS
Steady state portal venous pressure was increased by 102.2 (35.6)% (14.9 (3.6) mm Hg) and 272.3 (78.0)% (24.0 (2.2) mm Hg) above the basal pressure following sequential injections of 15 and 80 microns diameter microspheres, respectively. Sequential injection of 15, 40, and 80 microns diameter microspheres in either ascending or descending order of size did not generate further increases in portal venous pressure. A single injection of 1.8 x 10(5) 80 microns microspheres consistently produced a steady state portal venous pressure of 19.0 (1.3) mm Hg but did not approach the much higher value of 36.6 (43.2) mm Hg measured during clamping of the portal vein. These data indicate that the opening of patent intrahepatic shunts was responsible for the reduced pressures observed during microsphere injections and further evidence for this was provided by the location of microspheres in the pulmonary vascular bed. The elevation in portal venous pressure achieved by microsphere injections was not significantly different to that produced in rats subjected to partial portal vein ligation (20.7 (0.5) mm Hg, p > 0.05). Wedged hepatic venous pressure decreased from 6.7 (0.7) to 3.0 (0.6) mm Hg following injection of 80 microns microspheres, suggesting a decrease in total hepatic blood flow. Conversely, injection of 15 microns microspheres induced an increase in wedged hepatic venous pressure from 7.0 (1.0) mm Hg to 12.4 (1.8) mm Hg, indicating a localised redistribution of blood flow at the presinusoidal level of the portal venous vascular network and increased intrahepatic shunt flow.


CONCLUSIONS
It is suggested that there may be a protective pathophysiological role for these shunts when the liver is subjected to changes which induce acute portal hypertension.
Li
X
X
Department of Surgery, King's College School of Medicine and Dentistry, Rayne Institute, London, UK.
Benjamin
I S
IS
Alexander
B
B
D000208:Acute Disease; D000818:Animals; D006975:Hypertension, Portal / Q000473:pathology / Q000503:physiopathology*; D008099:Liver / Q000473:pathology; D008297:Male; D008863:Microspheres; D010477:Perfusion; D011168:Portal System; D051381:Rats; D017208:Rats, Wistar