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• W2171362937 abstract "Hypoxic pulmonary vasoconstriction is a common consequence of acute lung injury and may be mediated by increased local production of proinflammatory cytokines. Ethyl pyruvate is a novel anti-inflammatory agent that has been shown to down-regulate proinflammatory genes following hemorrhagic shock; however, its effects on hypoxic pulmonary vasoconstriction are unknown. We hypothesized that ethyl pyruvate would inhibit hypoxic pulmonary vasoconstriction and down-regulate pulmonary artery cytokine expression during hypoxia. To study this, isometric force displacement was measured in isolated rat pulmonary artery rings (n = 8/group) during hypoxia (95% N2/5% CO2) with or without prior ethyl pyruvate (10 mm) treatment. Following 60 min of hypoxia, pulmonary artery rings were analyzed for tumor necrosis factor-α and interleukin-1 mRNA via reverse transcriptase polymerase chain reaction. Ethyl pyruvate inhibited hypoxic pulmonary artery contraction (4.49 ± 2.32% versus 88.80 ± 5.68% hypoxia alone) and attenuated the hypoxic up-regulation of pulmonary artery tumor necrosis factor and interleukin-1 mRNA (P < 0.05). These data indicate that (1) hypoxia increases pulmonary artery vasoconstriction and proinflammatory cytokine gene expression; (2) ethyl pyruvate decreases hypoxic pulmonary vasoconstriction and down-regulates hypoxia-induced pulmonary artery proinflammatory cytokine gene expression; and (3) ethyl pyruvate may represent a novel therapeutic adjunct in the treatment of acute lung injury. Hypoxic pulmonary vasoconstriction is a common consequence of acute lung injury and may be mediated by increased local production of proinflammatory cytokines. Ethyl pyruvate is a novel anti-inflammatory agent that has been shown to down-regulate proinflammatory genes following hemorrhagic shock; however, its effects on hypoxic pulmonary vasoconstriction are unknown. We hypothesized that ethyl pyruvate would inhibit hypoxic pulmonary vasoconstriction and down-regulate pulmonary artery cytokine expression during hypoxia. To study this, isometric force displacement was measured in isolated rat pulmonary artery rings (n = 8/group) during hypoxia (95% N2/5% CO2) with or without prior ethyl pyruvate (10 mm) treatment. Following 60 min of hypoxia, pulmonary artery rings were analyzed for tumor necrosis factor-α and interleukin-1 mRNA via reverse transcriptase polymerase chain reaction. Ethyl pyruvate inhibited hypoxic pulmonary artery contraction (4.49 ± 2.32% versus 88.80 ± 5.68% hypoxia alone) and attenuated the hypoxic up-regulation of pulmonary artery tumor necrosis factor and interleukin-1 mRNA (P < 0.05). These data indicate that (1) hypoxia increases pulmonary artery vasoconstriction and proinflammatory cytokine gene expression; (2) ethyl pyruvate decreases hypoxic pulmonary vasoconstriction and down-regulates hypoxia-induced pulmonary artery proinflammatory cytokine gene expression; and (3) ethyl pyruvate may represent a novel therapeutic adjunct in the treatment of acute lung injury." @default.
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• W2171362937 date "2008-03-01" @default.
• W2171362937 modified "2023-09-26" @default.
• W2171362937 title "Ethyl Pyruvate Inhibits Hypoxic Pulmonary Vasoconstriction and Attenuates Pulmonary Artery Cytokine Expression" @default.
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• W2171362937 doi "https://doi.org/10.1016/j.jss.2007.03.067" @default.
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