Genetic deletion of NOS3 increases lethal cardiac dysfunction following mouse cardiac arrest

Resuscitation

Volumn 82, Issue 1, 2011, Pages 115-121

  Beiser, David G ^a   Orbelyan, Gerasim A ^a   Inouye, Brendan T ^a   Costakis, James G ^a   Hamann, Kimm J ^a   McNally, Elizabeth M ^a   Hoek, Terry L Vanden ^a  

^a UNIVERSITY OF CHICAGO   (United States)

Author keywords

Cardiopulmonary arrest; Cardiopulmonary resuscitation; Cyclic guanosine monophosphate; Nitric oxide; Nitric oxide synthase 3; Sudden cardiac arrest; Troponin I

Indexed keywords

CYCLIC GMP; ENDOTHELIAL NITRIC OXIDE SYNTHASE; HEMOGLOBIN; NITRIC OXIDE; POTASSIUM CHLORIDE; TROPONIN I;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; FEMALE; GENE DELETION; HEART ARREST; HEART DISEASE; HEART FUNCTION; HEART LEFT VENTRICLE PRESSURE; KNOCKOUT MOUSE; LETHALITY; MOUSE; MYOCARDIAL DISEASE; NITROSYLATION; NONHUMAN; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; RESUSCITATION; RETURN OF SPONTANEOUS CIRCULATION; SHOCK;

ANIMALS; BLOTTING, WESTERN; CARDIOPULMONARY RESUSCITATION; DISEASE MODELS, ANIMAL; DNA; FEMALE; GENE DELETION; HEART ARREST; MICE; MICE, INBRED C57BL; MYOCARDIUM; NITRIC OXIDE SYNTHASE TYPE III; VENTRICULAR DYSFUNCTION, LEFT;

EID: 78650766949     PISSN: 03009572     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.resuscitation.2010.08.038     Document Type: Article

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