Haemodynamic and ultrastructural observations on the rat liver after two‐thirds partial hepatectomy^*

Abstract

Rat liver ultrastructure was investigated after partial hepatectomy (PH), by scanning and transmission electron microscopy. Portal pressure was monitored before and after PH and, after killing performed at 6, 12, 24, 48 h and 10 d, regenerating livers were fixed by portal vein perfusion under haemodynamic conditions identical to those existing in vivo. An early and persistent increase in portal pressure after PH was found (P 0.01 for normal vs sham-operated controls). Ultrastructural study showed sinusoid dilatation and disappearance of the sieve-plate arrangement of small endothelial pores, thus leaving the parenchymal liver cell surface directly exposed to portal blood. Widening of sinusoids, endothelial fenestrations, intercellular spaces and spaces of Disse, was accompanied by dilatation of bile canaliculi. At 10 d, liver ultrastructure had returned to normal. Our observations suggest that a rise in portal pressure, as a consequence of PH, may be related to the observed ultrastructural changes in the liver.

Sinusoidal ultrastructure evaluated during the revascularization of regenerating rat liver

“…10,[33][34][35] At this time, we observed that fenestration diameter and porosity increases significantly in zone 1. Fenestration diameter does not increase as markedly in zone 3, and this could be a result of the pressure differences reported between the 2 zones.…”

“…36 Increased portal pressure resulting from 70% PHx has been shown to persist at least until 72 hr after resection. 10,34,35,37 Our results indicate that increased portal pressure is probably not the only effector of porosity, because increased porosity was not maintained throughout the reported period of elevated pressure (Figs. 1-3).…”

“…Fenestration diameter does not increase as markedly in zone 3, and this could be a result of the pressure differences reported between the 2 zones. 10,33 Rapid increases in portal pressures are suspected to contribute to fenestration diameters, because artificially high perfusion pressures have been shown to greatly enlarge fenestrations potentially damaging sieve plate structures. 36 Increased portal pressure resulting from 70% PHx has been shown to persist at least until 72 hr after resection.…”

“…(See also vitro and in vivo studies have also shown that fenestrae can modulate their diameter in response to soluble agents as well as a variety of environmental conditions, including changes in shear stress and portal pressure, and pathological ECM deposition. [10][11][12][13][14][15][16][17][18][19] We sought to investigate the trends in porosity expression in the SEC within and between lobule zones throughout the revascularization process following PHx. We believed that such changes may play a critical role in the sieving function of the sinusoids and contribute to the progression of the regenerative process.…”

“…9 Fenestrations are thought to regulate flow of these agents by modulating porosity throughout the sinusoidal wall. Therefore, fenestrations are not passive sieves, but are most probably very dynamic structures whose size and density have been shown to be affected by physical factors such as portal pressure and shear stress 10,11 ; soluble substances such as alcohol, 12 serotonin, 13 endotoxin, 14 and nicotine 15 ; and cytoskeletal disruption agents like cytochalasin B, 16,17 as well as the composition of the ECM. 18,19 Given the fact that SEC fenestrations can modulate their diameters in response to a variety of factors and events, we sought to examine fenestration size and sinusoidal porosity index with respect to ultrastructural changes taking place within the regenerating lobule.…”