NHE inhibition does not improve Na+ or Ca2+ overload during reperfusion: Using modeling to illuminate the mechanisms underlying a therapeutic failure

PLoS Computational Biology

Volumn 7, Issue 10, 2011, Pages

  Roberts, Byron N ^a   Christini, David J ^a  

^a WEILL CORNELL MEDICAL COLLEGE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM; PATHOLOGY; RESTORATION;

CA 2+; CARDIAC MYOCYTES; INTRACELLULAR SPACES; ISCHAEMIA; PROTON GRADIENT; REPERFUSION; REPERFUSION INJURY; REVERSE MODE; THERAPEUTIC FAILURE; TIME POINTS;

SODIUM;

ADENOSINE TRIPHOSPHATASE (POTASSIUM SODIUM); SODIUM CALCIUM EXCHANGE PROTEIN; SODIUM PROTON EXCHANGE PROTEIN; SODIUM;

ACIDOSIS; ANIMAL CELL; ANIMAL EXPERIMENT; ARTICLE; CALCIUM CELL LEVEL; CALCIUM TRANSPORT; CELL PH; CONTROLLED STUDY; DISEASE ACTIVITY; DISEASE SIMULATION; EXPERIMENTAL GUINEA PIG; HEART MUSCLE CELL; HEART MUSCLE ISCHEMIA; INTRACELLULAR SIGNALING; MATHEMATICAL COMPUTING; MATHEMATICAL MODEL; MOLECULAR DYNAMICS; MOLECULAR PATHOLOGY; NONHUMAN; OXIDATIVE STRESS; PROTON SODIUM EXCHANGE; PROTON TRANSPORT; REPERFUSION INJURY; SODIUM CELL LEVEL; SODIUM TRANSPORT; ANIMAL; BIOLOGICAL MODEL; COMPUTER SIMULATION; DRUG ANTAGONISM; HUMAN; METABOLISM; PH; PHYSIOLOGY; RAT; TREATMENT FAILURE;

ANIMALS; COMPUTER SIMULATION; HUMANS; HYDROGEN-ION CONCENTRATION; MODELS, CARDIOVASCULAR; MYOCARDIAL REPERFUSION INJURY; RATS; SODIUM; SODIUM-HYDROGEN ANTIPORTER; SODIUM-POTASSIUM-EXCHANGING ATPASE; TREATMENT FAILURE;

EID: 80055092197     PISSN: 1553734X     EISSN: 15537358     Source Type: Journal    
DOI: 10.1371/journal.pcbi.1002241     Document Type: Article

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