Reduced Brain Na+,K+-Atpase Activity During Acute Hepatic Failure in the Rat: a Possible Cause of Encephalopathy and Cerebral Oedema

1984 ◽  
Vol 66 (6) ◽  
pp. 62P.1-62P ◽  
Author(s):  
R.J. Ede ◽  
C.D. Gove ◽  
Roger Williams
1987 ◽  
Vol 72 (3) ◽  
pp. 365-371 ◽  
Author(s):  
Roland J. Ede ◽  
Christopher D. Gove ◽  
Robin D. Hughes ◽  
William Marshall ◽  
Roger Williams

1. Previously we have shown that sera from patients with fulminant hepatic failure (FHF) will inhibit partially purified rat brain Na+,K+-ATPase and sodium efflux from human leucocytes in vitro. Similar inhibition may be involved in the pathogenesis of encephalopathy and cerebral oedema in these patients. 2. In the present study we have attempted to establish whether the activity of brain Na+,K+-ATPase is decreased in vivo in rats with d-galactosamine induced hepatic failure using homogenates of snap-frozen brains. 3. Na+,K+-ATPase activity was significantly reduced in the forebrain region at the stage of mild encephalopathy (43 h after injection), while at the deeper stage of coma (43–53 h after injection) enzyme activity was further reduced in the forebrain region and was also significantly reduced in the hindbrain region. Ouabain insensitive ATPase activity was not significantly altered at any time. 4. While a significant increase in the water content (0.5%) of the hindbrain region was found 43 h after galactosamine, there was no clear correlation between the development of cerebral oedema and the reduction of Na+,K+-ATPase activity. 5. The activity of partially purified normal rat brain Na+,K+-ATPase was 15% lower when incubated with sera from rats in the deep stage of coma compared with control sera. 6. These data support other evidence that the reduction in brain Na+,K+-ATPase is likely to be due to toxic substance circulating in serum which have been shown to inhibit this enzyme in vitro and to cause coma when administered to normal animals.


2016 ◽  
Vol 0 (3.74) ◽  
pp. 112
Author(s):  
I.A. Kuchinskaya ◽  
M.V. Bondar ◽  
D.B. Areshnikov ◽  
S.S. Shapoval ◽  
R.D. Dobush

Critical Care ◽  
10.1186/cc560 ◽  
1999 ◽  
Vol 3 (Suppl 1) ◽  
pp. P187
Author(s):  
MC DaSilva ◽  
M Gupta ◽  
MJ Holman ◽  
HG Yang ◽  
RL Conter ◽  
...  

2004 ◽  
Vol 17 (3) ◽  
pp. 163-171 ◽  
Author(s):  
Nils R. Frühauf ◽  
Karl J. Oldhafer ◽  
Stephanie Westermann ◽  
Georgios C. Sotiropoulos ◽  
Gernot M. Kaiser

2000 ◽  
Vol 124 (12) ◽  
pp. 1800-1803 ◽  
Author(s):  
Marius J-M. Ilario ◽  
Jose E. Ruiz ◽  
Constantine A. Axiotis

Abstract Massive hepatic necrosis following exposure to phenytoin and trimethoprim-sulfamethoxazole is a rare occurrence and to the best of our knowledge has not been reported previously. Acute hepatic failure following administration of trimethoprim-sulfamethoxazole has rarely been seen, and only 4 cases have been well documented pathologically. We report a case of acute liver failure in a 60-year-old woman following ingestion of phenytoin and trimethoprim-sulfamethoxazole concomitantly over a 9-day period. Autopsy findings revealed acute fulminant hepatic failure. This case demonstrates the effects of chemical-chemical interactions in the potentiation of hepatotoxicity of single agents and specifically illustrates the need for discontinuing trimethoprim-sulfamethoxazole in the presence of early liver injury.


2018 ◽  
Vol 33 (1) ◽  
pp. 96
Author(s):  
Joo-Yun Kim ◽  
Hyun-Su Ri ◽  
Ji-Uk Yoon ◽  
Eun-Ji Choi ◽  
Hye-Jin Kim ◽  
...  

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