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脂氧素A4和脂氧素B4对豚鼠气道组织的收缩活性。

The contractile activities of lipoxin A4 and lipoxin B4 for guinea-pig airway tissues.

作者信息

Jacques C A, Spur B W, Crea A E, Lee T H

机构信息

Department of Medicine, United Medical School, Guy's Hospital, London.

出版信息

Br J Pharmacol. 1988 Oct;95(2):562-8. doi: 10.1111/j.1476-5381.1988.tb11677.x.

Abstract
  1. The isometric contractile activities of lipoxin A4 (LxA4) and lipoxin B4 (LxB4) were evaluated on guinea-pig lung tissue over the concentration range, 10(-8) to 10(-5) M. 2. LxA4 contracted guinea-pig lung parenchymal strips; the concentration eliciting 50% maximum histamine response was 3 x 10(-6) M. LxA4 did not contract tracheal spirals. 3. The LxA4 dose-response curve was parallel to that of leukotriene D4 (LTD4) with LxA4 being approximately 10,000 fold less potent than LTD4. 4. The time course of the contraction elicited by LxA4 was similar to that of LTD4 and it was slow in onset and did not plateau for 20 min. 5. Pre-incubation of parenchymal strips with leukotriene receptor antagonists at a concentration of 1 x 10(-6) M to 3 x 10(-5) M FPL 55712 or 3 x 10(-5) M L 649923 inhibited LxA4 activity. 6. Pre-incubation of tissues with 1 x 10(-5) M L 651392, a 5-lipoxygenase inhibitor, or 1 x 10(-5) M indomethacin, a cyclo-oxygenase inhibitor, did not affect the contractile activity of LxA4. 7. LxB4 did not constrict parenchymal strips or tracheal spirals.
摘要
  1. 在10⁻⁸至10⁻⁵M的浓度范围内,评估了脂氧素A4(LxA4)和脂氧素B4(LxB4)对豚鼠肺组织的等长收缩活性。2. LxA4使豚鼠肺实质条收缩;引起50%最大组胺反应的浓度为3×10⁻⁶M。LxA4未使气管螺旋条收缩。3. LxA4的剂量反应曲线与白三烯D4(LTD4)的平行,LxA4的效力比LTD4低约10000倍。4. LxA4引起的收缩时间进程与LTD4相似,起效缓慢,20分钟内未达到平台期。5. 用浓度为1×10⁻⁶M至3×10⁻⁵M的白三烯受体拮抗剂FPL 55712或3×10⁻⁵M的L 649923预孵育实质条可抑制LxA4活性。6. 用5-脂氧合酶抑制剂1×10⁻⁵M的L 651392或环氧化酶抑制剂1×10⁻⁵M的吲哚美辛预孵育组织,不影响LxA4的收缩活性。7. LxB4未使实质条或气管螺旋条收缩。

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本文引用的文献

6
Formation and actions of leukotrienes.白三烯的形成与作用。
Physiol Rev. 1984 Apr;64(2):744-61. doi: 10.1152/physrev.1984.64.2.744.
8
Heterogeneity of leukotriene receptors in guinea-pig trachea.豚鼠气管中白三烯受体的异质性。
Prostaglandins. 1983 Feb;25(2):171-8. doi: 10.1016/0090-6980(83)90102-8.

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