Altering hydrodynamic variables influences PGI2 production by isolated lungs and endothelial cells.
Altering hydrodynamic variables influences PGI2 production by isolated lungs and endothelial cells.
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改变流体动力学变量会影响离体肺和内皮细胞的 PGI2 产生。
DOI：
10.1152/jappl.1984.57.2.388
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Voelkel,NF
中科院分区：
文献类型：
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作者：
vanGrondelle,A;Worthen,GS;Ellis,D;Mathias,MM;Murphy,RC;Strife,RJ;Reeves,JT;Voelkel,NF
由于肺组织的变形刺激前列腺素的合成，我们想研究流体动力是否会影响肺前列环素（PGI 2）的生产。为了检验肺前列环素合成是流量依赖性的假设，我们检测了流量改变后肺前列环素的产生。使用含有Ficoll或白蛋白的盐溶液作为灌注液，我们将流量改为对照流量的一半并加倍。当流量改变时，肺前列环素的产生跟随流量和压降的变化。当用吲哚美辛治疗的肺中流量变化时，前列环素的产生太低而无法测量。恒定平均流量下压力脉动的变化对肺前列环素的产生没有影响。由于血管扩张也可能刺激前列环素的产生，我们增加了静脉压。静脉压的增加（从2.1到4.8毫米汞柱）对前列环素的产生没有影响;静脉压的进一步增加（到7.5毫米汞柱）引发水肿，并导致前列环素产生的大量增加。当我们将单层内皮细胞培养在威尔斯孔中，以确定的剪切速率，前列环素浓度在上清液中迅速增加到最大值。没有进一步增加与更大的剪切可能反映了前列环素合成的反馈控制。结果表明，流体动力学干扰影响内皮细胞，刺激花生四烯酸代谢。肺前列环素的产生可能与血流有关。然而，与水肿形成期间肺前列环素的产生相比，这种影响很小。
Because deformation of lung tissue stimulates prostaglandin synthesis, we wanted to investigate whether hydrodynamic forces would affect lung prostacyclin (PGI2) production. To test the hypothesis that lung prostacyclin synthesis was flow dependent, we examined lung prostacyclin production after flow alterations. Using a salt solution that contained either Ficoll or albumin as a perfusate, we changed the flow to half and to double the control flow. When flow was changed, lung prostacyclin production followed changes in flow and pressure drop. When flow was varied in lungs treated with indomethacin, prostacyclin production was too low to be measurable. Variations in pressure pulsatility at constant mean flow had no influence on lung prostacyclin production. Since vascular distension may also stimulate prostacyclin production, we increased venous pressure. An increase in venous pressure (from 2.1 to 4.8 mmHg) had no effect on prostacyclin production; a further increase in venous pressure (to 7.5 mmHg) initiated edema and caused a large increase in prostacyclin production. When we subjected monolayers of endothelial cells cultured in wells to defined shear rates, the prostacyclin concentration in the supernatant quickly increased to a maximum. The absence of further increase with greater shear may have reflected feedback control of prostacyclin synthesis. The results indicated that hydrodynamic disturbances affect endothelial cells and stimulate arachidonate metabolism. Lung prostacyclin production may be related to flow. However, this effect is small compared with the lung prostacyclin production during edema formation.