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Role of renal sympathetic nerve activity in renal failure associated with obstructive jaundice in the rat

The propensity for renal failure associated with obstructive jaundice and liver disease may be related to enhanced vasoconstriction of the renal vascular bed with resultant decreases in renal blood flow. Renal sympathetic nervous activity may be a mediator of this effect. The increased renal product... Full description

Journal Title: The American journal of surgery 1991, Vol.161 (6), p.662-667
Main Author: O'Neill, Patricia A
Other Authors: Wait, Richard B , Kahng, Kim U
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: New York, NY: Elsevier Inc
ID: ISSN: 0002-9610
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recordid: cdi_proquest_miscellaneous_80721646
title: Role of renal sympathetic nerve activity in renal failure associated with obstructive jaundice in the rat
format: Article
creator:
  • O'Neill, Patricia A
  • Wait, Richard B
  • Kahng, Kim U
subjects:
  • 6-Ketoprostaglandin F1 alpha - urine
  • Abridged Index Medicus
  • Animals
  • Bile Ducts - surgery
  • Biological and medical sciences
  • Cholestasis - physiopathology
  • Denervation
  • Dinoprostone - urine
  • Kidney - innervation
  • Kidney - metabolism
  • Kidney Failure, Chronic - physiopathology
  • Kidney Failure, Chronic - urine
  • Kidney Function Tests
  • Ligation
  • Male
  • Medical sciences
  • Nephrology. Urinary tract diseases
  • Prostaglandins - metabolism
  • Rats
  • Rats, Inbred Strains
  • Sympathetic Nervous System - physiopathology
  • Thromboxane B2 - urine
ispartof: The American journal of surgery, 1991, Vol.161 (6), p.662-667
description: The propensity for renal failure associated with obstructive jaundice and liver disease may be related to enhanced vasoconstriction of the renal vascular bed with resultant decreases in renal blood flow. Renal sympathetic nervous activity may be a mediator of this effect. The increased renal production of prostaglandins which has been observed in previous models of bile duct ligation may serve to counterbalance the effects of such vasoconstricting influences. This study was undertaken to assess the effect of bile duct ligation on renal function and prostaglandin production in the rat. Furthermore, this study was designed to determine if renal sympathetic nerve activity contributes to the development of renal failure after bile duct ligation. Sprague-Dawley rats underwent either sham operation (n = 8), bilateral renal denervation (n = 10), bile duct ligation alone (n = 11), or bile duct ligation and bilateral renal denervation (n = 10). Renal function was assessed before and 4 days after operation. Bile duct ligation resulted in a 46% decrease in creatinine clearance (p
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0002-9610
fulltext: fulltext
issn:
  • 0002-9610
  • 1879-1883
url: Link


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titleRole of renal sympathetic nerve activity in renal failure associated with obstructive jaundice in the rat
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descriptionThe propensity for renal failure associated with obstructive jaundice and liver disease may be related to enhanced vasoconstriction of the renal vascular bed with resultant decreases in renal blood flow. Renal sympathetic nervous activity may be a mediator of this effect. The increased renal production of prostaglandins which has been observed in previous models of bile duct ligation may serve to counterbalance the effects of such vasoconstricting influences. This study was undertaken to assess the effect of bile duct ligation on renal function and prostaglandin production in the rat. Furthermore, this study was designed to determine if renal sympathetic nerve activity contributes to the development of renal failure after bile duct ligation. Sprague-Dawley rats underwent either sham operation (n = 8), bilateral renal denervation (n = 10), bile duct ligation alone (n = 11), or bile duct ligation and bilateral renal denervation (n = 10). Renal function was assessed before and 4 days after operation. Bile duct ligation resulted in a 46% decrease in creatinine clearance (p <0.01), a 33% decrease in urinary sodium excretion (p <0.01), a twofold increase in urine flow (p <0.01), and twofold increases in urinary excretion of PGE 2, 6-keto-PGF 1α, and thromboxane B 2 (p <0.01). Renal denervation did not prevent the decreases in creatinine clearance and sodium excretion seen after bile duct ligation and had no effect on the changes in urine flow and prostaglandin excretion. These findings demonstrate that bile duct ligation in the rat results in impaired renal function, accompanied by increases in renal prostaglandin production. In addition, this study indicates that the perturbations in renal function and renal prostaglandin production induced by bile duct ligation are not mediated by renal sympathetic nerve activity.
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subject6-Ketoprostaglandin F1 alpha - urine ; Abridged Index Medicus ; Animals ; Bile Ducts - surgery ; Biological and medical sciences ; Cholestasis - physiopathology ; Denervation ; Dinoprostone - urine ; Kidney - innervation ; Kidney - metabolism ; Kidney Failure, Chronic - physiopathology ; Kidney Failure, Chronic - urine ; Kidney Function Tests ; Ligation ; Male ; Medical sciences ; Nephrology. Urinary tract diseases ; Prostaglandins - metabolism ; Rats ; Rats, Inbred Strains ; Sympathetic Nervous System - physiopathology ; Thromboxane B2 - urine
ispartofThe American journal of surgery, 1991, Vol.161 (6), p.662-667
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descriptionThe propensity for renal failure associated with obstructive jaundice and liver disease may be related to enhanced vasoconstriction of the renal vascular bed with resultant decreases in renal blood flow. Renal sympathetic nervous activity may be a mediator of this effect. The increased renal production of prostaglandins which has been observed in previous models of bile duct ligation may serve to counterbalance the effects of such vasoconstricting influences. This study was undertaken to assess the effect of bile duct ligation on renal function and prostaglandin production in the rat. Furthermore, this study was designed to determine if renal sympathetic nerve activity contributes to the development of renal failure after bile duct ligation. Sprague-Dawley rats underwent either sham operation (n = 8), bilateral renal denervation (n = 10), bile duct ligation alone (n = 11), or bile duct ligation and bilateral renal denervation (n = 10). Renal function was assessed before and 4 days after operation. Bile duct ligation resulted in a 46% decrease in creatinine clearance (p <0.01), a 33% decrease in urinary sodium excretion (p <0.01), a twofold increase in urine flow (p <0.01), and twofold increases in urinary excretion of PGE 2, 6-keto-PGF 1α, and thromboxane B 2 (p <0.01). Renal denervation did not prevent the decreases in creatinine clearance and sodium excretion seen after bile duct ligation and had no effect on the changes in urine flow and prostaglandin excretion. These findings demonstrate that bile duct ligation in the rat results in impaired renal function, accompanied by increases in renal prostaglandin production. In addition, this study indicates that the perturbations in renal function and renal prostaglandin production induced by bile duct ligation are not mediated by renal sympathetic nerve activity.
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06-Ketoprostaglandin F1 alpha - urine
1Abridged Index Medicus
2Animals
3Bile Ducts - surgery
4Biological and medical sciences
5Cholestasis - physiopathology
6Denervation
7Dinoprostone - urine
8Kidney - innervation
9Kidney - metabolism
10Kidney Failure, Chronic - physiopathology
11Kidney Failure, Chronic - urine
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13Ligation
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15Medical sciences
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17Prostaglandins - metabolism
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21Thromboxane B2 - urine
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abstractThe propensity for renal failure associated with obstructive jaundice and liver disease may be related to enhanced vasoconstriction of the renal vascular bed with resultant decreases in renal blood flow. Renal sympathetic nervous activity may be a mediator of this effect. The increased renal production of prostaglandins which has been observed in previous models of bile duct ligation may serve to counterbalance the effects of such vasoconstricting influences. This study was undertaken to assess the effect of bile duct ligation on renal function and prostaglandin production in the rat. Furthermore, this study was designed to determine if renal sympathetic nerve activity contributes to the development of renal failure after bile duct ligation. Sprague-Dawley rats underwent either sham operation (n = 8), bilateral renal denervation (n = 10), bile duct ligation alone (n = 11), or bile duct ligation and bilateral renal denervation (n = 10). Renal function was assessed before and 4 days after operation. Bile duct ligation resulted in a 46% decrease in creatinine clearance (p <0.01), a 33% decrease in urinary sodium excretion (p <0.01), a twofold increase in urine flow (p <0.01), and twofold increases in urinary excretion of PGE 2, 6-keto-PGF 1α, and thromboxane B 2 (p <0.01). Renal denervation did not prevent the decreases in creatinine clearance and sodium excretion seen after bile duct ligation and had no effect on the changes in urine flow and prostaglandin excretion. These findings demonstrate that bile duct ligation in the rat results in impaired renal function, accompanied by increases in renal prostaglandin production. In addition, this study indicates that the perturbations in renal function and renal prostaglandin production induced by bile duct ligation are not mediated by renal sympathetic nerve activity.
copNew York, NY
pubElsevier Inc
pmid1862825
doi10.1016/0002-9610(91)91251-D