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Endothelin‐1–induced vasoconstriction causes a significant increase in portal pressure of rat liver: Localized constrictive effect on the distal segment of preterminal portal venules as revealed by light and electron microscopy and serial reconstruction
Author(s) -
Kaneda Kenji,
Ekataksin Wichai,
Sogawa Mitsue,
Matsumura Akiko,
Cho Akikuni,
Kawada Norifumi
Publication year - 1998
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510270315
Subject(s) - constriction , lumen (anatomy) , anatomy , perfusion , vasoconstriction , portal venous pressure , contraction (grammar) , medicine , microvessel , venule , pathology , portal hypertension , chemistry , microcirculation , immunohistochemistry , cirrhosis
Intraportal infusion of endothelin‐1 (ET‐1), a potent vasoconstrictor, significantly elevates portal venous pressure. To determine the major site of vascular constriction in the intrahepatic porto‐sinusoidal system, we performed an in situ perfusion of rat livers with 1 nmol/L ET‐1 at a flow rate of 20 mL/min. Portal pressure rose from 22 cm H 2 O to 54 cm H 2 O within 25 minutes. Specimens were prepared for light‐microscopic serial reconstruction and electron microscopy. The distal segment of preterminal portal venules (DS/PPV) with an inner diameter of 40 to 80 μm showed complete obliteration of the lumen over a 300‐μm distance caused by the intense contraction of perivascular smooth muscle cells and protruding of endothelial cells into the lumen. The proximal segment of preterminal portal venules (PS/PPV) with a larger diameter up to 150 μm also underwent strong constriction, but still had luminal space for the flow, while the PS/PPV with a diameter of 150 to 400 μm showed moderate or mild constriction and retained a wide lumen. Neither terminal portal venules, inlet venules, sinusoids, nor central veins, however, exhibited demonstrable constriction. Liver parenchyma fed by the inlet venules that emerged from the PS/PPV exhibited a wide sinusoidal lumen and vacuolated hepatocytes caused by the influx of excess portal perfusate that escaped from the occlusive areas. The present study has revealed that the DS/PPV functions as a presinusoidal quasi‐sphincter mechanism and is involved in the redistribution of intrahepatic portal flow under increased portal pressure.