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TRIACSIN C, A FATTY ACYL COA SYNTHETASE (FACS) INHIBITOR, IMPROVES CARDIAC PERFORMANCE FOLLOWING GLOBAL ISCHEMIA
Author(s) -
Weis Margaret Teresa,
Tolson Jasmine,
Chen Qian,
Young Lindon
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1136.18
Subject(s) - enos , ischemia , medicine , cardiology , reperfusion injury , pharmacology , nitric oxide , nitric oxide synthase
Extensive evidence shows that eNOS is protective in ischemia/reperfusion (I/R) injury. We have shown that triacsin C, a (FACS) inhibitor, increases eNOS activity in the post‐ischemic rat hind limb, suggesting that triacsin C might be useful in treatment of cardiac I/R. Isolated rat hearts, perfused at a constant pressure by the method of Langendorf, were subjected to a 30 minute period of global ischemia, followed by 45 minutes of reperfusion in the presence or absence of 5μM triacsin C. At 45 minutes of reperfusion, LVDP and dP/dt in treated hearts were significantly better than in vehicle controls. Coronary flow and heart rate were not changed by treatment. The infarct area, visualized with 1% 2,3,5‐triphenylterazolium, was significantly smaller in triacsin C treated hearts. The results support the hypothesis, and suggest that FACS inhibitors may represent a new category of drugs for I/R.