Mitochondrial dysfunction and cytoskeletal disruption during chemical hypoxia to cultured rat hepatic sinusoidal endothelial cells: The pH paradox and cytoprotection by glucose, acidotic pH, and glycine

Hepatology

Volumn 27, Issue 4, 1998, Pages 1039-1049

  Nishimura, Yoshiya ^a   Romer, Lewis H ^a,b   Lemasters, John J ^a  

^a UNIVERSITY OF NORTH CAROLINA   (United States)

^b UNIVERSITY OF NORTH CAROLINA SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ACTIN; ADENOSINE TRIPHOSPHATE; GLUCOSE; GLYCINE; POTASSIUM CYANIDE;

ACIDIFICATION; ANIMAL CELL; ARTICLE; CELL CULTURE; CELL DEATH; CELL HYPOXIA; CELL PROTECTION; CONTROLLED STUDY; CYTOSKELETON; ENDOTHELIUM CELL; LIVER MITOCHONDRION; LIVER SINUSOID; MALE; MEMBRANE DEPOLARIZATION; MEMBRANE POTENTIAL; MITOCHONDRIAL MEMBRANE; NONHUMAN; PH; PRIORITY JOURNAL; RAT; REPERFUSION INJURY; REPOLARIZATION;

ADENOSINE TRIPHOSPHATE; ANIMALS; CELL HYPOXIA; CELLS, CULTURED; CYCLOSPORINE; CYTOPROTECTION; CYTOSKELETON; ENDOTHELIUM, VASCULAR; GLUCOSE; GLYCINE; HYDROGEN-ION CONCENTRATION; MALE; MEMBRANE POTENTIALS; MITOCHONDRIA, LIVER; RATS; RATS, SPRAGUE-DAWLEY; REPERFUSION INJURY;

EID: 0031899906     PISSN: 02709139     EISSN: None     Source Type: Journal    
DOI: 10.1002/hep.510270420     Document Type: Article

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