Hepatic venular pressures of rats, dogs, and rabbits

H. G. Bohlen, R. Maass-Moreno, C. F. Rothe

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

We tested the hypotheses that the hepatic venule pressures (P(hv)), just downstream from the hepatic sinusoids, are closely similar (<2 mmHg) either to the portal venous pressure (P(pv)), indicating a high hepatic venous resistance, or to the inferior vena cava (P(ivc)) pressure, indicating a high portal-sinusoidal venous resistance, as reported by previous investigators. A micropipette servo-null pressure measurement technique was used with rats, dogs, and rabbits. P(hv), referred to the anatomic level of the vena cava, averaged 5.1 ± 1.0, 6.4 ± 1.1, and 5.4 ± 1.0 (SD) mmHg in the rats, puppies, and rabbits, respectively. P(pv) averaged 8.0 ± 1.4, 10.8 ± 2.2, and 7.4 ± 1.5 mmHg, respectively. Norepinephrine infusion into the portal vein (1-5 μg·min-1·kg-1) caused P(pv) to increase and the portal venous flow to decrease but did not significantly affect P(hv). The hepatic venous circuit contributed 44 ± 17% (rats) and 31 ± 26% (dogs) of the total liver venous vascular resistance under control conditions. We conclude that the portal and sinusoidal vasculatures are the dominant, but not exclusive, resistance sites of the liver venous vasculature both at rest and during norepinephrine-induced vasoconstriction.

Original languageEnglish (US)
Pages (from-to)G539-G547
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume261
Issue number3 24-3
DOIs
StatePublished - 1991

Keywords

  • Hepatic venules
  • Liver
  • Nonrepinephrine
  • Vascular resistance

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)

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