Effect of cyclooxygenase inhibition on ethchlorvynol-induced acute lung injury in dogs.
Effect of cyclooxygenase inhibition on ethchlorvynol-induced acute lung injury in dogs.
复制标题
环氧合酶抑制对乙氯维诺诱导的狗急性肺损伤的影响。
DOI：
10.1152/jappl.1986.61.3.1058
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Lonigro,AJ
中科院分区：
文献类型：
--
作者：
Sprague,RS;Stephenson,AH;Dahms,TE;Lonigro,AJ
在麻醉犬中，选择性地将乙基氯维醇（ECV，9 mg/kg）注入右肺循环，产生以非流体静力性肺水肿和全身低氧血症为特征的单侧急性肺损伤（ALI）。为了研究环氧合酶活性产物是动脉低氧血症的介质而不是该损伤中的水肿形成的假设，在ECV给药之前，用两种化学上不同的环氧合酶抑制剂之一，吲哚美辛（5 mg/kg）或布洛芬（12.5 mg/kg）或溶剂（0.1 M碳酸钠）对动物进行预处理。用任一抑制剂预处理防止在用溶剂预处理的动物中观察到的ECV诱导的全身低氧血症（P小于0.01）。尽管有这种全身氧合的保护，但在单侧ECV给药后，没有血流重新分布到未损伤的肺。在ALI之前抑制环氧合酶并不能减少肺水的积聚。在布洛芬组，左心房压力显着增加后ECV管理。我们的结论是，环氧合酶介导的花生四烯酸代谢的产品（S）是负责改变血管反应性和随之而来的全身低氧血症在这个模型中，但水肿形成后ECV是不相关的环氧合酶活性。此外，在诱导ALI之前给药的布洛芬表现出与吲哚美辛不同的性质，但在减轻低氧血症的能力或限制水肿形成的失败方面没有不同。
In anesthetized dogs ethchlorvynol (ECV, 9 mg/kg) was selectively administered into the right pulmonary circulation to produce unilateral acute lung injury (ALI) characterized by nonhydrostatic pulmonary edema and systemic hypoxemia. To investigate the hypothesis that products of cyclooxygenase activity are mediators of the arterial hypoxemia, but not the edema formation in this injury, animals were pretreated with one of two chemically dissimilar cyclooxygenase inhibitors, indomethacin (5 mg/kg), or ibuprofen (12.5 mg/kg), or vehicle (0.1 M sodium carbonate) prior to the administration of ECV. Pretreatment with either inhibitor prevented the ECV-induced systemic hypoxemia observed in animals pretreated with vehicle (P less than 0.01). Despite this protection of systemic oxygenation, there was no redistribution of blood flow to the uninjured lung following unilateral ECV administration. Cyclooxygenase inhibition prior to ALI did not attenuate the accumulation of lung water. In the ibuprofen group, left atrial pressure increased significantly following ECV administration. We conclude that a product(s) of cyclooxygenase-mediated arachidonic acid metabolism is responsible for the altered vascular reactivity and consequent systemic hypoxemia in this model, but that the edema formation following ECV is not related to cyclooxygenase activity. In addition, ibuprofen, administered prior to the induction of ALI, exhibits properties not shared by indomethacin but is not different in its capacity to attenuate hypoxemia or in its failure to limit edema formation.