PROSTANOIDS CONTRIBUTE TO ACETAMINOPHEN INDUCED VASCULAR DYSFUNCTION IN RATS
AbstractAcetaminophen (APAP) is the most consumed potentially toxic drug in the world, and its cardiovascular injury has been emphasized. We evaluated the role of inflammatory mediators in the impaired vascular relaxation after APAP treatment. Rats were treated with APAP for 2 weeks (400 mg/Kg/day/p.o.) and after euthanasia, blood was collected for biochemical analysis (hepatic transaminases, lipid peroxidation and glutathione), and aortas were isolated for vascular reactivity, lipid peroxidation and biochemical analysis (glutathione, arachidonic acid, TBXA2, PGD2, 12-HETE and 15-HETE). Both blood and arteries presented increased levels of lipid peroxidation and decreased levels of glutathione. The vasodilation response to acetylcholine was impaired in the APAP group and restored after treatment with diclofenac (10 μM). In the arteries, levels of arachidonic acid were reduced while PGD2 was increased (TBXA2, 12- and 15-HETE remained significantly unchanged). Thus, oxidative stress and contractile prostanoids play a significant role in the impaired vascular relaxation caused by APAP treatment.
Article Information
10
1365-1370
710 KB
506
English
IJPSR
Hellen Karine Paes Porto, Mikaelle Costa Correia, Marcella Daruge Grando and Matheus Lavorenti Rocha *
Laboratory of Cardiovascular Pharmacology, Faculty of Pharmacy, Federal University of Goias, Goiânia/GO - Brazil.
rochaml@ufg.br.
10 November 2023
10 January 2024
05 April 2024
10.13040/IJPSR.0975-8232.15(5).1365-70
01 May 2024
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