灌注心脏中受体介导的白三烯释放的调节
Modulation of receptor mediated leukotriene release in the perfused heart.
作者信息
Lefer A M, Roth D M, Kugler J L, Smith J B
出版信息
Gen Pharmacol. 1986;17(4):437-40. doi: 10.1016/0306-3623(86)90187-4.
The chemotactic peptide n-formyl-methionyl-leucyl-phenylalanine (FMLP) induces peptide leukotriene release at concentrations of 20-25 pmol/ml 3 min after the start of FMLP infusion. FMLP-induced leukotriene release in rabbit hearts is not blocked by the leukotriene receptor antagonist FPL-55712 at concentrations that totally antagonize the hemodynamic effects of exogenously infused peptide leukotrienes. Moreover, propyl gallate, a lipoxygenase inhibitor, does not block FMLP-induced leukotriene release. However, the chemotactic peptide antagonist (Boc-Phe-Leu-Phe-Leu-Phe-OH) totally antagonized FMLP-induced leukotriene release suggesting that the release is via a different mechanism, possibly a receptor mediated event.
趋化肽N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸（FMLP）在开始输注FMLP 3分钟后，浓度为20 - 25 pmol/ml时可诱导肽白三烯释放。在兔心脏中，FMLP诱导的白三烯释放不受白三烯受体拮抗剂FPL - 55712的阻断，该拮抗剂在完全拮抗外源性输注肽白三烯的血流动力学效应的浓度下也无此作用。此外，脂氧合酶抑制剂没食子酸丙酯也不能阻断FMLP诱导的白三烯释放。然而，趋化肽拮抗剂（Boc - Phe - Leu - Phe - Leu - Phe - OH）可完全拮抗FMLP诱导的白三烯释放，这表明该释放是通过不同机制进行的，可能是一个受体介导的事件。
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