[在离体犬叶前列腺素抑制剂存在下的肺血管反应性和水肿的发展]。

A Palomar Lever, N A González Montero, R Fernández Capistrán, A Gómez González, R Harari Ancona, M L Martínez Guerra, J Sandoval Zárate, L Oppenheimer
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引用次数: 0

摘要

未标示:肺泡缺氧是最强大的肺血管收缩剂。在之前的工作中,我们没有证明在肺泡缺氧的情况下,孤立犬叶模型的血管反应性和水肿形成有显著变化。本研究的目的是明确使用前列腺素抑制剂如tiaprofenic acid和肺泡缺氧诱导肺血管收缩后血管肺反应性和水肿的形成。对6只离体犬肺小叶进行了测量和研究,它们均在两种条件下(常氧FIO2 21%和缺氧FIO2 5%), 4只在常氧条件下开始,2只在缺氧条件下开始。结果:肺组织滤过率无明显变化,常氧0.42 +/- 0.41,缺氧0.37 +/- 0.51 ml/min/100 g P = NS。基础条件下动脉压为25.1 +/- 6.21,缺氧时动脉压升高至37 +/- 7.19 cm H2O (δ 12.0 +/- 1.2 cm H2O)。P < 0.001。结论:经tiaprofenic acid预处理的离体犬肺叶缺氧血管反应性明显增强,肺通透性无明显变化,水肿发生率无明显增高。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Pulmonary vascular reactivity and the development of edema in the presence of prostaglandin inhibitors in the isolated canine lobe].

Unlabelled: Alveolar hypoxia is the most powerful pulmonary vasoconstrictor. In a previous work, we did not demonstrate significant changes in vascular reactivity and edema formation in an isolated canine lobe model during alveolar hypoxia. The purpose of this study is to define vascular pulmonary reactivity and edema formation after induction of pulmonary vasoconstriction using a prostaglandin inhibitor like tiaprofenic acid and alveolar hypoxia. Six isolated canine pulmonary lobules were instrumented and studied, all of them under two conditions (normoxia FIO2 21% and hypoxia FIO2 5%) four starting in normoxia condition and 2 starting in hypoxia condition.

Results: No significant changes in filtration rate were found, normoxia 0.42 +/- 0.41, hypoxia 0.37 +/- 0.51 ml/min/100 g pulmonary tissue P = NS. The arterial pressure in basal conditions was 25.1 +/- 6.21, and during hypoxia increased to 37 +/- 7.19 cm H2O (Delta 12.0 +/- 1.2 cm H2O). P < 0.001.

Conclusion: Hypoxia vascular reactivity was significantly increased in tiaprofenic acid pretreated isolated canine lobes, no changes in pulmonary permeability was found nor increased rate in edema formation.

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