We have reported that PGE
1 enhances bile flow by increasing bile canalicular contractions through Ca
++-calmodulin-actomyosin system. The present study was designed to elucidate the effects and action sites of PGE
1 on the hepatic microvasculature at the sinusoidal level. Male Wistar strain male were used. PGE
1 was continuously infused for 1hr at 50ng/min/100g b.w. through a mesenteric vein catheter. Hepatic sinusoidal blood flow was measured by laser Doppler flowmetry before and after the beginning of PGE
1 infusion. The sinusoidal endothelial fenestrae (SEF) were observed by scanning electron microscopy. The ultrastructal localizations of the Ca
++-ATPase activity were observed in rat liver treated with or without PGE
1 by electron cytochemical method of Ando. Hepatic sinusoidal blood flow (before: 39.02±23.23ml/min/100g, after 15min: 55.16±2.36, p<0.05) were increased by PGE
1 infusion with no changes in portal venous pressure and systemic arterial pressure. Morphometric analysis revealed that the SEF were significantly increased in diameter in zone 1 of the PGE
1 infused livers (control: 98.2±42.7nm, PGE
1-infused: 279.7±158.3nm, p<0.001). By transmission microscopy, the microfilaments were evident in the subplasmalemmal region and around the SEF in the hepatic sinusoidal endothelium. These filaments were specifically decorated with heavy meromyosin, providing evidence that they were actin filaments. The Ca
++-ATPase activity identified on the sinusoidal endothelial plasma membranes was increased by the portal infusion of PGE
1 via a mesenteric vein catheter. In conclusion PGE
1 causes an increase in hepatic sinusoidal blood flow, at least in part, by the relaxation of hepatic sinusoidal endothelial cells, i.e. the actin filamentst-mediated dilatation of SEF possibly due to the extrusion of intracytoplasmic free Ca
++-through the activation of Ca
++-pump ATPase on the plasma membranes.
View full abstract