Infarct size-reducing effect of nicorandil is mediated by the K(ATP) channel but not by its nitrate-like properties in dogs

Cardiovascular Research

Volumn 32, Issue 2, 1996, Pages 274-285

  Mizumura, Tsuneo ^a   Nithipatikom, Kasem ^a   Gross, Garrett J ^a  

^a MEDICAL COLLEGE OF WISCONSIN   (United States)

Author keywords

Adenosine; ATP sensitive; Dog, anesthetized; Infarct size; Myocardial infarction; Nicorandil; Nitroglycerin; Potassium channel; Potassium channel openers; Sulphonylureas

Indexed keywords

ADENOSINE; GLIBENCLAMIDE; GLYCERYL TRINITRATE; GUANYLATE CYCLASE; METHYLENE BLUE; NICORANDIL; POTASSIUM CHANNEL; SULFONYLUREA DERIVATIVE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CONTROLLED STUDY; DISEASE SEVERITY; DOG; DRUG MECHANISM; FEMALE; HEART INFARCTION SIZE; HEART PROTECTION; INTRAARTERIAL DRUG ADMINISTRATION; INTRACARDIAC DRUG ADMINISTRATION; INTRAVENOUS DRUG ADMINISTRATION; MALE; NONHUMAN; PRIORITY JOURNAL;

ADENOSINE; ANIMALS; DOGS; FEMALE; GLYBURIDE; ION CHANNEL GATING; MALE; METHYLENE BLUE; MYOCARDIAL INFARCTION; MYOCARDIAL REPERFUSION; MYOCARDIUM; NIACINAMIDE; NICORANDIL; NITRIC OXIDE; NITROGLYCERIN; POTASSIUM CHANNELS; VASODILATOR AGENTS;

EID: 0030222372     PISSN: 00086363     EISSN: None     Source Type: Journal    
DOI: 10.1016/0008-6363(96)00061-2     Document Type: Article

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