作者: Jean-François Bouchard , Daniel Lamontagne
DOI: 10.1097/00005344-199911000-00019
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摘要: Summary: The aim of this study was to assess whether cyclooxygenase (COX) inhibitors protect the endothelial function against deleterious effect ischemia and reperfusion. Isolated rat hearts perfused under constant-flow conditions were exposed 30 min partial (flow, 1 ml/min) followed by 20 reperfusion, after which coronaries precontracted with U-46619, response endothelium-dependent vasodilator, serotonin (5-HT), compared that endothelium-independent sodium nitroprusside (SNP). In untreated hearts, diminished selectively 5-HT-induced vasodilation, sham (without ischemia). vasodilation SNP unaffected in all groups. Pretreatment 6-MNA, µM, a COX-2 inhibitor some activity on COX 1, diclofenac, µM (COX-1 -2), or 1-(7-carboxyheptyl) imidazole, 10 [thromboxane (TX) synthase inhibitor] but not indomethacin, inhibitor) preserved induced 5-HT ischemia. Enzyme immunoassays indicated decreased concentration TXB2 6-keto-PGF1[alpha] [stable metabolites TXA2 prostacyclin (PGI2), respectively] coronary effluent during Furthermore, indomethacin only one abolish PGE2 early No clear trend ventricular postischemic recovery could be observed between treated groups our experimental protocols. These data suggest that, conditions, 1-7-CHI, via reduction TX concentration. Disparities may due complete abolition reperfusion group.