Hepatorenal reflex in the rat

Meredith, Todd A.; Brand, Paul H.; Metting, Patricia J.; Britton, Steven L.

doi:10.1139/y-97-162

Cited by 5 publications

(3 citation statements)

References 27 publications

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“…Iwao et alÕs results 35 and ours should also be compared to Jalan et alÕs study, 22 which suggests the role of the hepatorenal reflex 21,39,40 in cirrhotic patients. In Jalan et alÕs study, a significant decrease in renal blood flow followed an acute increase in portal pressure secondary to intrahepatic portosystemic stent-shunt occlusion.…”

Section: Discussionsupporting

confidence: 55%

Changes in renal artery resistance after meal‐induced splanchnic vasodilatation in cirrhotic patients

Perney

Taourel

Gallix

et al. 2001

J of Clinical Ultrasound

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Section: Discussionsupporting

confidence: 55%

Changes in renal artery resistance after meal‐induced splanchnic vasodilatation in cirrhotic patients

Perney

Taourel

Gallix

et al. 2001

J of Clinical Ultrasound

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“…In normal circumstances, hepatic osmoreceptors will detect a high sodium diet and will cause a decrease in renal sympathetic nervous activity by the hepatorenal osmoreflex, which results in an increased diuresis and urinary sodium excretion (Carlson et al, 1998). The decrease in renal sympathetic nervous activity is lost after liver denervation, resulting in sodium retention and an increase in blood pressure (Ishiki et al, 1991; Morita et al, 1993; Meredith et al, 1997; Carlson et al, 1998). This happens especially after a high but also after a low sodium diet (Morita et al, 1995; Meredith et al, 1997; Carlson et al, 1998).…”

Section: Effect Of Hepatic Denervation In Experimental Animal Modelsmentioning

confidence: 99%

“…The decrease in renal sympathetic nervous activity is lost after liver denervation, resulting in sodium retention and an increase in blood pressure (Ishiki et al, 1991; Morita et al, 1993; Meredith et al, 1997; Carlson et al, 1998). This happens especially after a high but also after a low sodium diet (Morita et al, 1995; Meredith et al, 1997; Carlson et al, 1998). Hepatic denervated rats have a 12 mm Hg higher mean arterial blood pressure than sham rats (Carlson et al, 1998).…”

Section: Effect Of Hepatic Denervation In Experimental Animal Modelsmentioning

confidence: 99%

Transplanted liver: Consequences of denervation for liver functions

et al. 2004

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Following liver transplantation, all hepatic nerves are transected; thus, liver allografts are completely isolated from neural control of their hosts. Despite this absolute denervation, liver allograft function does not appear to be significantly impaired after successful transplantation. In experimental animal models, hepatic denervation has no major effects on bile acid production and biotransformation, while it increases blood pressure and salt retention; decreases the number of hepatic progenitor cells, cholangiocyte proliferation, and liver regeneration; and influences the hepatic microcirculation, diet behavior, and glycemic control. In humans, hepatic denervation after liver transplantation has no major deleterious effects on bile secretion, liver regeneration, and hepatic blood flow. Insulin resistance and postprandial hyperglycemia, changes in ingestion behavior, and reduced stimulation of hepatic progenitor cells in the canals of Hering are the major side effects of absent liver innervation. Despite these abnormalities, patients can lead a new life with improved quality of life. © 2004 Wiley-Liss, Inc. Key words: liver transplantation; denervation; function; hepaticLiver transplantation is the ultimate treatment for patients with acute fulminant and chronic liver failure. The results of liver transplantation are good, with a 1-year survival of 90 -95% and a 10-year survival of 50 -60%. Because of a shortage in cadaveric donors, living-related liver transplantation is a good option to overcome this problem.The autonomic nerves of the liver are formed by an anterior plexus (around the hepatic artery) and a posterior plexus (surrounds portal vein and bile duct). Parasympathetic nerves are derived from the vagus nerve and the sympathetic fibers from the celiac ganglion. Sensory nerve endings are present in the liver capsule, central veins, and bile ducts. Most of the afferent nerves from the liver run via the vagus and splanchnic nerves, but some also to the right phrenic nerve. The afferent nerves register information from nocireceptors, osmo-and baroreceptors, as well as ionic and metabolic receptors (Bathal and Grossman, 1999).Following liver transplantation, the hepatic nerves are inevitably transected below the porta hepatis or at the hepatoduodenal ligament; thus, liver allografts are completely isolated from the neural control of their hosts. Despite this absolute denervation, the liver allograft does not appear to be significantly compromised after successful transplantation. There is no obvious deficiency in the regulation of liver metabolism (production of proteins such as albumin and coagulation factors, metabolization) and bile production. At first blush, it seems that under normal circumstances, hormones and substrates reaching the liver by circulation are responsible for control of the organ function, and that the role of hepatic nerves is mainly restricted to situations of physiological stress.However, a more profound search revealed that hepatic denervation has a lot of consequences...

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