Changes in Hepatic Hemodynamics due to Primary Liver Tumours

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.

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Recovery of blood flow and oxygen transport after temporary ischemia of rat liver

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1998.275.1.h243 ◽

1998 ◽

Vol 275 (1) ◽

pp. H243-H249 ◽

Cited By ~ 1

Author(s):

Hiromu Kazuo ◽

Toshirou Nishida ◽

Akitoshi Seiyama ◽

Shigeyuki Ueshima ◽

Eisaku Hamada ◽

...

Keyword(s):

Blood Flow ◽

Hepatic Artery ◽

Hepatic Blood Flow ◽

Tissue Perfusion ◽

Hepatic Tissue ◽

Tissue Blood Flow ◽

Initial Increase ◽

Transport Parameters ◽

Artery Ligation ◽

Venous Flow

Hepatic tissue perfusion and O2 supply after ischemia are indispensable for recovery of cellular functions, but few studies have been performed regarding the recovery of tissue blood flow and O2 transport. After 5, 15, and 30 min of ischemia of rat livers, hepatic tissue perfusion, hepatic arterial and portal blood flow, plasma[Formula: see text], and O2 transport parameters were measured. Hepatic tissue blood flow and erythrocyte velocity in the sinusoids showed biphasic recoveries after temporal ischemia for 5, 15, and 30 min. The first peak in the flow appeared at 3–4 min after the initiation of tissue perfusion, and the second peak appeared at ∼20 min, irrespective of the ischemic period. Hepatic blood flow during the initial increase contained relatively low O2-saturated blood compared with that in the second increase. Livers that had been subjected to a prior hepatic artery ligation only showed the first peak at ∼4 min. The first increase in hepatic blood flow corresponded to the peak in the portal venous flow, and the second increase corresponded to that of the hepatic artery. These results suggested that hepatic microcirculation after temporary hepatic ischemia showed biphasic recoveries because of different restoration patterns of the portal vein and hepatic artery.

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Factors influencing control of arterial circulation in the liver of the dog

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1963.205.6.1260 ◽

1963 ◽

Vol 205 (6) ◽

pp. 1260-1264 ◽

Cited By ~ 40

Author(s):

Roy Cohn ◽

Samuel Kountz

Keyword(s):

Blood Flow ◽

Hepatic Artery ◽

Artery Blood Flow ◽

Portal Venous Flow ◽

Hepatic Arterial Flow ◽

Experimental Conditions ◽

Venous Flow ◽

Arterial Circulation ◽

Factors Influencing ◽

Intrinsic Regulation

Measurements were made of the hepatic arterial flow in thirty-one mongrel dogs by the use of the electromagnetic square wave flowmeter under the following experimental conditions: hepatic arterial neurectomy, portal venous flow reductions, portal venous flow elimination and diversion, and systemic acidosis and alkalosis. The findings suggest that the periarterial nerves about the hepatic artery influence the intrinsic regulation of hepatic artery blood flow only in the presence of severely reduced portal venous flow.

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

Laboratory Animals ◽

10.1177/00236772211000370 ◽

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.

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General anesthesia and hepatic circulation

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-276 ◽

1987 ◽

Vol 65 (8) ◽

pp. 1762-1779 ◽

Cited By ~ 94

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.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1998.274.3.h777 ◽

1998 ◽

Vol 274 (3) ◽

pp. H777-H785 ◽

Cited By ~ 9

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.

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