Location and function of intrahepatic shunts in anaesthetised rats

Abstract

Background: In the present study we determined the proportion of shunt flow due to patent intrahepatic portal systemic shunts in the normal rat liver and its relationship with microsphere induced portal hypertension. Methods: Systemic and hepatic haemodynamics were measured continuously before, during, and after intraportal injection of 15 µm diameter microspheres in anaesthetised male Wistar rats. Functional hepatic blood flow and intrahepatic shunt flow were determined by the use of constant intraportal infusion of sorbitol and simultaneous measurements in the portal vein, hepatic vein, and carotid artery. The percentage of large shunts of diameter >15 µm were estimated by intraportal injection of 51 Cr labelled 15 µm diameter microspheres. Results: Hepatic sorbitol uptake was 97.9 (0.5)% in normal control rats, with functional hepatic blood flow equalling total hepatic blood flow (2.52 (0.23) ml/min/100 g body weight). Microsphere injection decreased sorbitol uptake to 12.8 (4.3)% and further to 4.1 (0.7)% when followed by hepatic arterial ligation. In the latter two groups, intrahepatic shunt flow (1.46 (0.15) and 1.16 (0.19) ml/min/100 g body weight, respectively) was not significantly different from portal venous flow (1.36 (0.20) and 1.20 (0.20) ml/min/100 g body weight, respectively). Portal venous flow remained at 70% of basal values and portal venous pressure only increased by 50% from baseline. 51 Cr labelled microsphere shunt fraction through large shunts (>15 µm) was less than 1.0%. Conclusion: The site of confluence between the hepatic artery and portal vein is in zone II. Intrahepatic shunts originate in presinusoidal regions in zone I in the normal liver and, when activated by intraportal injection of microspheres, divert 70% of the total portal blood flow away from zone III and thereby reduce acute increases in portal venous pressure.

Lymphatic and portal vein absorption of organochlorine compounds in rats

“…Three animals were euthanized after 24 h and 3 animals, after 48 h. Samples of blood were taken from the heart. The distribution of 14 C between plasma and RBCs was measured, and 85 Ϯ 3.1% was found in the red cells in the 24-h sample and 87 Ϯ 2.6%, after 48 h. This affinity of HCB for RBC membranes is consistent with the report of Gomez-Catalan and coworkers (4). Preliminary study of the appearance of HCB in tissues of lymph-diverted rats.…”

“…Assumptions of flow rate and volume are needed to estimate portal vein absorption with this methodology. Portal blood flow rate can be measured by methods with ultrasound or electromagnetic flowmeter (3,14). This measurement is not within the scope of our studies; however, it is not necessary for our calculations.…”

“…Two additional rats were fitted with a mesenteric lymph cannula (to provide chylomicrons to recipient animals) as reported previously (8) and gastrically intubated with 1 ml of olive oil containing 10 Ci of [ 14 C]HCB and 50 Ci of [ 3 H]triolein. The animals were euthanized at the completion of the lymphatic collection, and tissues were analyzed for 14 C and 3 H. We found markedly higher concentrations of HCB relative to that of triolein in the tissues of both animals. The concentration of HCB was 4 -11 times higher in the liver and 60 -200 times higher in the fat pad.…”

“…In each tissue the concentration of 14 Table 3. The distribution of 14 C among the lipoprotein fractions is presented in Fig. 5.…”

A Novel Canine Model of Portal Vein Stenosis Plus Thioacetamide Administration-Induced Cirrhotic Portal Hypertension With Hypersplenism

“…Portal venous flow (PVF), hepatic arterial flow (HAF), and velocity of portal blood flow were measured by ALC-Ultrasonic Blood Flow System (Shanghai Alcott Biotech Co. Ltd. China). Portal venous resistance (PVR) was then calculated as PVP/PVF (mmHg/ ml/min/kg body weight) [19].…”