Preservation of mitochondrial function during ischemia as a possible mechanism for cardioprotection of diltiazem against ischemia/reperfusion injury

Biochemical Pharmacology

Volumn 67, Issue 3, 2004, Pages 565-574

  Takeo, Satoshi ^a   Tanonaka, Kouichi ^a   Iwai, Takeshi ^a   Motegi, Kanataka ^a   Hirota, Yuko ^a  

^a TOKYO UNIVERSITY OF PHARMACY AND LIFE SCIENCES   (Japan)

Author keywords

Diltiazem; Heart; Ischemia; Mitochondria; Na + overload; Na+ channels

Indexed keywords

5 (N ETHYL N ISOPROPYL)AMILORIDE; ADENOSINE TRIPHOSPHATE; CYTOCHROME C; DILTIAZEM; LACTATE SODIUM; OXYGEN; PHOSPHATE; SODIUM CHANNEL; SODIUM CHANNEL BLOCKING AGENT; SODIUM CHLORIDE; SODIUM ION; SODIUM PROTON EXCHANGE PROTEIN; TETRODOTOXIN;

ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BIOACCUMULATION; CONTROLLED STUDY; CONVALESCENCE; CULTURE MEDIUM; CYTOSOL; DRUG EFFECT; DRUG MECHANISM; ENERGY; ENERGY YIELD; HEART FUNCTION; HEART LEFT VENTRICLE PRESSURE; HEART MITOCHONDRION; HEART MUSCLE CONTRACTILITY; HEART MUSCLE ISCHEMIA; HEART MUSCLE PERFUSION; HEART MUSCLE REPERFUSION; HEART PROTECTION; MALE; MITOCHONDRIAL RESPIRATION; NONHUMAN; OXYGEN CONSUMPTION; PRIORITY JOURNAL; PROTEIN SECRETION; RAT; REPERFUSION INJURY;

EID: 1242286139     PISSN: 00062952     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.bcp.2003.09.016     Document Type: Article

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