The relationship between intrahepatic portal systemic shunts andmicrosphere induced portal hypertension in the rat liver

Background—Portal hypertension is associated withgross haemodynamic disturbances characterised by high cardiac output,low peripheral vascular resistance, increased splanchnic blood flow, and portal systemic shunting.
Aims—To study the relationship betweenintrahepatic portal systemic shunts and microsphere induced portalhypertension in the rat liver.
Methods—Different sized microspheres weresequentially injected into the portal vein of male Wistar rats.
Results—Steady state portal venous pressure wasincreased 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 µm diameter microspheres, respectively. Sequential injection of 15, 40, and 80 µm 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× 10⁵ 80 µm microspheres consistently produced a steadystate portal venous pressure of 19.0 (1.3) mm Hg but did not approachthe 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 observedduring microsphere injections and further evidence for this wasprovided by the location of microspheres in the pulmonary vascular bed.The elevation in portal venous pressure achieved by microsphereinjections was not significantly different to that produced in ratssubjected 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) mmHg following injection of 80 µm microspheres, suggesting a decreasein total hepatic blood flow. Conversely, injection of 15 µmmicrospheres induced an increase in wedged hepatic venous pressure from7.0 (1.0) mm Hg to 12.4(1.8) mm Hg, indicating a localisedredistribution of blood flow at the presinusoidal level of the portalvenous vascular network and increased intrahepatic shunt flow.
Conclusion—It is suggested that there may be aprotective pathophysiological role for these shunts when the liver issubjected to changes which induce acute portal hypertension.