Anatomy of efferent hepatic nerves

2004 ◽  
Vol 280A (1) ◽  
pp. 821-826 ◽  
Author(s):  
Robert S. McCuskey
Keyword(s):  
1980 ◽  
Vol 238 (5) ◽  
pp. R390-R394 ◽  
Author(s):  
D. R. Kostreva ◽  
A. Castaner ◽  
J. P. Kampine

The reflex effects of hepatic low-pressure baroreceptors on renal and cardiopulmonary sympathetic efferent nerve activity were studied in mongrel dogs anesthetized with pentobarbital sodium. Systemic blood pressure, central venous pressure, hepatic, renal, and portal venous pressures were all measured during occlusion of the thoracic vena cava above the diaphragm, below the liver, and during occlusion of the portal vein. Renal and cardiopulmonary sympathetic efferent nerve activity was continuously recorded along with the hepatic efferent nerve activity during the caval occlusions. Hepatic baroreceptor excitation resulted in marked increases in hepatic afferent nerve activity and reflex increases in renal and cardiopulmonary sympathetic efferent nerve activity without a change in heart rate. Section of the anterior hepatic nerves eliminated the reflex increase in renal efferent nerve activity, but did not eliminate the increase in cardiopulmonary sympathetic efferent nerve activity. Carotid sinus denervation, bilateral cervical vagotomy, and phrenectomy did not alter the reflex responses to hepatic baroreceptor excitation. These hepatorenal and hepatocardiopulmonary reflexes may be important reflex mechanisms that are activated during congestive heart failure and cirrhosis of the liver.


1977 ◽  
Vol 232 (6) ◽  
pp. H652-H656
Author(s):  
W. W. Lautt

Acute denervation of the liver did not result in changes of oxygen uptake or hemodynamics in the intact liver of the cat. Stimulation of the hepatic nerves resulted in a marked reduction of vascular conductance of the hepatic artery and portal vein (intrahepatic) resulting in almost complete cessation of arterial flow and increased portal blood pressure. The hepatic artery showed a more complete escape from the neurogenic vasoconstriction than did the portal vein. During the stable "escape phase" oxygen delivery was 86% of control, but hepatic extraction of oxygen increased so that oxygen uptake was not altered from control values. The return of oxygen consumption to normal during nerve stimulation suggests that redistribution of hepatic blood flow did not occur. In spite of arterial and portal venous blood pressure changes and changes in gut conductance, oxygen extraction of the gut did not change.


1997 ◽  
Vol 273 (6) ◽  
pp. E1194-E1202 ◽  
Author(s):  
Thomas O. Mundinger ◽  
C. Bruce Verchere ◽  
Denis G. Baskin ◽  
Michael R. Boyle ◽  
Stephan Kowalyk ◽  
...  

Stimulation of canine hepatic nerves releases the neuropeptide galanin from the liver; therefore, galanin may be a sympathetic neurotransmitter in the dog liver. To test this hypothesis, we used immunocytochemistry to determine if galanin is localized in hepatic sympathetic nerves and we used hepatic sympathetic denervation to verify such localization. Liver sections from dogs were immunostained for both galanin and the sympathetic enzyme marker tyrosine hydroxylase (TH). Galanin-like immunoreactivity (GALIR) was colocalized with TH in many axons of nerve trunks as well as individual nerve fibers located both in the stroma of hepatic blood vessels and in the liver parenchyma. Neither galanin- nor TH-positive cell bodies were observed. Intraportal 6-hydroxydopamine (6-OHDA) infusion, a treatment that selectively destroys hepatic adrenergic nerve terminals, abolished the GALIR staining in parenchymal neurons but only moderately diminished the GALIR staining in the nerve fibers around blood vessels. To confirm that 6-OHDA pretreatment proportionally depleted galanin and norepinephrine in the liver, we measured both the liver content and the hepatic nerve-stimulated spillover of galanin and norepinephrine from the liver. Pretreatment with 6-OHDA reduced the content and spillover of both galanin and norepinephrine by >90%. Together, these results indicate that galanin in dog liver is primarily colocalized with norepinephrine in sympathetic nerves and may therefore function as a hepatic sympathetic neurotransmitter.


1978 ◽  
Vol 235 (2) ◽  
pp. H262-H265
Author(s):  
W. W. Lautt ◽  
C. Wong ◽  
J. S. Durham ◽  
P. Taillon

A method for obtaining pure, mixed hepatic venous blood is described and evaluated in anesthetized cats. Hepatic vascular congestion does not occur with this “intracaval cannulation”, however small elevations in central venous blood pressure were noted. Although these changes persisted they did not result in systemic vascular congestion, judging from the normal arterial and portal pressures and from the lack of progressive decrease in arterial blood pressure. Blood samples obtained using the intracaval cannulation were shown to contain identical levels of oxygen as those obtained using a more complex surgical preparation. Reflux of blood from the vena cava does not occur during sampling. The responsiveness of this sampling method to rapid changes in venous content was evaluated by following the changes in glucose balance caused by direct stimulation of the hepatic nerves. The responses measured were similar to those measured in a separate set of experiments obtained using blood samples from a surgically isolated hepatic venous supply.


1995 ◽  
Vol 54 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Hironobu Morita ◽  
Qing-hui Chen ◽  
Hiroshi Hosomi

1969 ◽  
Vol 25 (3) ◽  
pp. 277-284 ◽  
Author(s):  
Clive V. Greenway ◽  
Ronald D. Stark ◽  
W. Wayne Lautt

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