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• W2000966970 abstract "Release of inflammatory mediators within the ischemic myocardium has long been thought to contribute to myocardial damage and dysfunction. Myocardial infarction (MI) and congestive heart failure (CHF) were induced in rats by ligating the left coronary artery. Animals were treated with the selective cyclooxygenase-2 (COX-2) inhibitor-5,5-dimethyl-3-(3-fluorophenyl1)-4-(4-methyl-sulphonyl-2(5H)-fluranone (DFU), low-, high-dose acetyl salicylic acid (aspirin), or vehicle for 3 months. Strong immunoreactivity for COX-2 was detected in the cardiomyocytes, vascular endothelial cells, and macrophages in the infarcted myocardium. Compared to the vehicle, treatment with DFU significantly reduced left ventricular end-diastolic pressure, central venous pressure, lung wet/dry ratio and infarct size, and improved cardiac contractility (P < 0.05). In comparison, treatment with low or high doses of aspirin did not significantly impact any of these parameters. These findings demonstrate that induction of myocardial COX-2 in rats with CHF secondary to MI contributes to the cardiac injury and dysfunction associated with this disease, and that therapy aimed at inhibiting this enzymatic pathway at the onset of the disease may be beneficial in the treatment of MI and CHF." @default.
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• W2000966970 date "2004-07-01" @default.
• W2000966970 modified "2023-09-26" @default.
• W2000966970 title "Inhibition of COX pathway in experimental myocardial infarction" @default.
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• W2000966970 doi "https://doi.org/10.1016/j.yjmcc.2004.04.002" @default.
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