Hepatic venular resistance responses to norepinephrine, isoproterenol, adenosine, histamine, and ACh in rabbits

1998 ◽  
Vol 274 (3) ◽  
pp. H777-H785 ◽  
Author(s):  
Carl F. Rothe ◽  
Roberto Maass-Moreno
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Blood Flow ◽  
Inferior Vena ◽  
Liver Volume ◽  
Liver Lobe ◽  
Inferior Vena Caval ◽  
Total Hepatic Blood Flow ◽  
Constant Rate ◽  
Increased Blood Flow

Changes in hepatic venous resistance were estimated in rabbits from the hepatic venular-inferior vena caval pressure gradient [servo-null micropipettes in 49 ± 15 (SD) μm vessels] and the total hepatic blood flow (ultrasound probe encircling the hepatic artery and the portal vein). Changes in liver volume, and thus vascular capacitance, were estimated from measures of the liver lobe thickness. Norepinephrine (NE), isoproterenol (Iso), adenosine (Ado), histamine (Hist), or acetylcholine (ACh) was infused into the portal vein at a constant rate for 5 min. NE, Hist, and Ado increased hepatic venular pressure, but only NE and Hist significantly increased hepatic venular resistance. NE reduced the liver thickness, but Hist and Ado caused engorgement. Hepatic blood flow was increased by NE and Ado and decreased by ACh. The influence of intraportal vein infusion of Iso on the liver vasculature, at doses similar to that of NE, was insignificant. We conclude that NE acted on all the hepatic microvasculature, increasing resistance and actively decreasing vascular volume. Hist passively induced engorgement by increasing outflow resistance, whereas the liver engorgement seen with Ado was passively related to the increased blood flow. ACh constricted the portal venules but did not change the liver volume.

Active and passive liver microvascular responses from angiotensin, endothelin, norepinephrine, and vasopressin

2000 ◽  
Vol 279 (3) ◽  
pp. H1147-H1156 ◽  
Author(s):  
Carl F. Rothe ◽  
Roberto Maass-Moreno
Keyword(s):  
Control Period ◽  
Liver Volume ◽  
Vena Cava ◽  
Ang Ii ◽  
Liver Lobe ◽  
Arterial Blood ◽  
Total Hepatic Blood Flow ◽  
Constant Rate ◽  
Inferior Vena Cava Pressure ◽  
Capacitance Vessels

Vasoconstrictor agents may induce a decrease in hepatic vascular volume passively, by decreasing distending pressure, or actively, by stimulating contractile elements of capacitance vessels. Hepatic venular resistance was estimated in anesthetized rabbits from hepatic venular pressure (Pμhv; by servo-null micropipette), inferior vena cava pressure, and total hepatic blood flow (Fhv; by ultrasound flow probe). Changes in liver volume were estimated from measures of liver lobe thickness. Angiotensin (ANG) II, endothelin (ET)-1, norepinephrine (NE), and vasopressin (VP) were infused into the portal vein at a constant rate for 5 min. We conclude that ANG II and NE induced active constriction of hepatic capacitance vessels, because the liver lobe thickness decreased significantly even though Pμhv and portal venous distending pressure (Ppv) increased. All four agents increased splanchnic and hepatic venous resistances in similar proportions. With VP, Pμhv and Ppv decreased, but with ET-1, Pμhv and Ppv increased. However, lobe thickness was not significantly changed by either drug during the infusion compared with the 2-min control period. Thus VP and ET-1 have only minor effects on hepatic capacitance vessels. ET-1, at 0.04 μg · min−1 · kg body wt−1, caused an increase in systemic arterial blood pressure, but erythrocyte movement through the sinusoids in some animals stopped.

Hepatic blood flow in adult Göttingen minipigs and pre-pubertal Danish Landrace x Yorkshire pigs

2021 ◽  
pp. 002367722110003
Author(s):  
Kristoffer Kjærgaard ◽  
Michael Sørensen ◽  
Frank Viborg Mortensen ◽  
Aage Kristian Olsen Alstrup
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Hepatic Blood Flow ◽  
Liver Tissue ◽  
Blood Perfusion ◽  
Flow Measurements ◽  
Total Hepatic Blood Flow ◽  
The Mean ◽  
Blood Flow Measurements

The liver receives dual blood supply from the hepatic artery and portal vein. The pig is often used as an animal model in positron emission tomography (PET) and pharmacokinetic studies because of the possibility for extensive and direct blood sampling. In this study, we compared measurements of hepatic blood flow in 10 female adult Göttingen minipigs and 10 female pre-pubertal Danish Landrace x Yorkshire (DLY) pigs. Ultrasound transit time flow meter probes were placed around the hepatic artery and portal vein through open surgery, hepatic blood flow measurements were performed, and the liver was weighed. Total hepatic blood flow was on average 363 ± 131 mL blood/min in Göttingen minipigs and 988 ± 180 mL blood/min in DLY pigs ( p < 0.001). The mean hepatic blood perfusion was 623 mL blood/min/mL liver tissue and 950 mL blood/min/mL liver tissue ( p = 0.005), and the liver weight was 0.58 kg and 1.04 kg, respectively. The mean arterial flow fraction in Göttingen minipigs was 12 ± 7% and lower than in DLY pigs, where it was 24 ± 7% ( p = 0.001). Using the gold standard for blood flow measurements, we found that both total hepatic blood flow and blood perfusion were significantly lower in Göttingen minipigs than in DLY pigs. The hepatic blood perfusion and arterial flow fraction in DLY pigs were comparable to normative values from humans. Differences in hepatic blood flow between adult Göttingen minipigs and humans should be considered when performing physiological liver studies in this model.

The Clearance of 133Xenon from the Liver Intraportal Injection in Man

1965 ◽  
Vol 05 (03) ◽  
pp. 241-245 ◽  
Author(s):  
K.-F. Aronsen ◽  
B. Ericsson ◽  
A. Fajgelj ◽  
S.-E. Lindell
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Blood Flow ◽  
Scintillation Detectors ◽  
Disappearance Rate ◽  
Simultaneous Measurements

Summary 133Xe dissolved in saline was injected into the portal vein in man. Hepatic blood flow was calculated from the disappearance rate of 133Xe recorded with scintillation detectors placed over the liver. The results are discussed and related to simultaneous measurements of the pressure in the portal vein.

scholarly journals Changes in Hepatic Hemodynamics due to Primary Liver Tumours

HPB Surgery ◽  
1996 ◽  
Vol 9 (4) ◽  
pp. 245-248 ◽  
Author(s):  
F. Jakab ◽  
Z. Ráth ◽  
F. Schmal ◽  
P. Nagy ◽  
J. Faller
Keyword(s):  
Hepatocellular Carcinoma ◽  
Blood Flow ◽  
Hepatic Artery ◽  
Hepatic Blood Flow ◽  
Primary Hepatocellular Carcinoma ◽  
Portal Venous Flow ◽  
Venous Flow ◽  
Control Value ◽  
Early Results ◽  
Total Hepatic Blood Flow

Data regarding the afferent circulation of the liver in patients with primary hepatocellular carcinoma are controversial, we have carried out measurement of hepatic arterial and portal venous flow intraoperatively by transit time ultrasonic volume flowmetry. In patients with primary hepatocellular carcinoma the hepatic artery flow increased to 0.55±0.211 compared with the control value of 0.37±0.102 1/min. (p<0.01). The portal venous flow decreased from 0.61±0.212 l/min, to 0.47±l/min. p<0.01). Due to the opposite changes in the afferent circulation the total hepatic blood flow did not change significantly, compared with controls.The ratio of hepatic arterial flow to portal vein flow increased to 1.239±0.246 in patients with hepatocellular carcinoma, which is double of the control value (0.66±0.259 l/min). After resection this ratio did not change.The resection did not alter hepatic artery or portal venous flow significantly, although the total hepatic blood flow decreased significantly (p<0.01).On the basis of our early results it is possible that the ratio of the two circulations may be to deel measured with doppler ultrasound and provide diagnostic information.

General anesthesia and hepatic circulation

1987 ◽  
Vol 65 (8) ◽  
pp. 1762-1779 ◽  
Author(s):  
Simon Gelman
Keyword(s):  
Blood Flow ◽  
General Anesthesia ◽  
Surgical Procedures ◽  
Hepatic Blood Flow ◽  
Portal Blood Flow ◽  
Arterial Blood Flow ◽  
Hepatic Circulation ◽  
Arterial Blood ◽  
Total Hepatic Blood Flow ◽  
Circulatory Disturbances

This article describes hepatic circulatory disturbances associated with anesthesia and surgical intervention. The material is presented in three parts: part 1 describes the effects of general anesthetics on the hepatic circulation; part 2 deals with different factors related to surgical procedures and anesthesia; and part 3 analyzes the role of hepatic circulatory disturbances and hepatic oxygen deprivation in anesthesia-induced hepatotoxicity. The analysis of available data suggests that general anesthesia affects the splanchnic and hepatic circulation in various directions and to different degrees. The majority of anesthetics decreases portal blood flow in association with a decrease in cardiac output. However, hepatic arterial blood flow can be preserved, decreased, or increased. The increase in hepatic arterial blood flow, when it occurs, is usually not enough to compensate for a decrease in portal blood flow and therefore total hepatic blood flow is usually decreased during anesthesia. This decrease in total hepatic blood flow-has certain pharmacokinetic implications, namely a decrease in clearance of endogenous and exogenous substances with a high hepatic extraction ratio. On the other hand, a reduction in the hepatic oxygen supply might play a certain role in liver dysfunction occurring perioperatively. Surgical procedures–preparations combined with anesthesia have a very complex effect on the splanchnic and hepatic circulation. Within this complex, the surgical procedure–preparation plays the main role in developing circulatory disturbances, while anesthesia plays only a modifying role. Hepatic oxygen deprivation may play an important role in anesthesia-induced hepatotoxicity in different experimental models.

Hepatic blood flow in experimental hemorrhagic shock

1962 ◽  
Vol 202 (1) ◽  
pp. 7-11 ◽  
Author(s):  
Edward D. Frank ◽  
Howard A. Frank ◽  
Stanley W. Jacob ◽  
Jacob Fine
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Hemorrhagic Shock ◽  
Hepatic Vein ◽  
Hepatic Blood Flow ◽  
Marked Reduction ◽  
Blood Replacement ◽  
Transient Improvement ◽  
Experimental Hemorrhagic Shock

In dogs in hemorrhagic shock, the blood flow and oxygenation of the liver were measured with a catheter in a hepatic vein. There is a marked reduction in hepatic blood flow and oxygenation throughout hemorrhagic shock. There is transient improvement following blood replacement and additional transfusions. Arterial shunts into the portal vein may restore hepatic oxygenation to preshock levels. Norepinephrine does not increase hepatic blood flow even though arterial pressure is restored to normal. Dibenamine pretreatment sustains the hepatic flow to some extent during hypovolemia; antibiotic pretreated animals do not differ from controls.

Evidence for the association between total hepatic blood flow and hepatic glutathione content

1986 ◽  
Vol 35 (10) ◽  
pp. 1629-1632 ◽  
Author(s):  
Walter G. Bottje ◽  
Aslam S. Hassan ◽  
Kenneth R. Holmes
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Total Hepatic Blood Flow ◽  
Hepatic Glutathione

Is it feasible to monitor total hepatic blood flow by use of transesophageal echography? An experimental study in pigs

2001 ◽  
Vol 27 (3) ◽  
pp. 580-585 ◽  
Author(s):  
Wolfram Schütz ◽  
Rainer Meierhenrich ◽  
Karl Träger ◽  
Albrecht Gauss ◽  
Peter Radermacher ◽  
...  
Keyword(s):  
Experimental Study ◽  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Total Hepatic Blood Flow
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