Hepatic venular pressures of rats, dogs, and rabbits
| Autor: | R. Maass-Moreno, C. F. Rothe, H. G. Bohlen |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
Male
medicine.medical_specialty Physiology Portal venous pressure Hemodynamics Blood Pressure Inferior vena cava Muscle Smooth Vascular Norepinephrine Dogs Species Specificity Venules Physiology (medical) Internal medicine medicine Animals Venule Hepatology Portal Vein business.industry Models Cardiovascular Gastroenterology Rats Inbred Strains Rats Surgery medicine.anatomical_structure Blood pressure medicine.vein Circulatory system Cardiology Vascular resistance Vascular Resistance Rabbits medicine.symptom business Vasoconstriction Liver Circulation |
| Zdroj: | American Journal of Physiology-Gastrointestinal and Liver Physiology. 261:G539-G547 |
| ISSN: | 1522-1547 0193-1857 |
| DOI: | 10.1152/ajpgi.1991.261.3.g539 |
| Popis: | We tested the hypotheses that the hepatic venule pressures (Phv), just downstream from the hepatic sinusoids, are closely similar (less than 2 mmHg) either to the portal venous pressure (Ppv), indicating a high hepatic venous resistance, or to the inferior vena cava (Pivc) 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. Phv, 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. Ppv averaged 8.0 +/- 1.4, 10.8 +/- 2.2, and 7.4 +/- 1.5 mmHg, respectively. Norepinephrine infusion into the portal vein (1-5 micrograms.min-1.kg-1) caused Ppv to increase and the portal venous flow to decrease but did not significantly affect Phv. 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. |
| Databáze: | OpenAIRE |
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