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吸入臭氧对血管内皮代谢功能及通气功能的影响。

The effect of ozone inhalation on metabolic functioning of vascular endothelium and on ventilatory function.

作者信息

Gross K B, White H J, Sargent N E

机构信息

Biomedical Science Department, General Motors Research Laboratories, Warren, Michigan 48090.

出版信息

Toxicol Appl Pharmacol. 1991 Jun 15;109(2):336-51. doi: 10.1016/0041-008x(91)90180-m.

Abstract

The primary purpose of this research was to determine the effect of ozone inhalation on pulmonary vascular endothelium. Male Fischer-344 rats were exposed to 0.5 or 0.7 ppm ozone, 20 hr/day for 7 days. Lungs were excised and perfused with Krebs medium containing [14C]serotonin or [14C]hippurylhistidylleucine (HHL). When compared to controls, the animals exposed to the lower ozone concentration showed no statistically significant changes in serotonin removal. In contrast, the higher ozone concentration resulted in a 32% decrease (p less than 0.0001) in serotonin removal, but had no effect on HHL. Rats similarly exposed to 0.7 ppm ozone but allowed to recover for 14 days in clean air showed no decrease in serotonin removal compared to their controls. Animals exposed sequentially to 0.5 ppm ozone for 7 days and then to 0.7 ppm for 7 days showed no alteration in serotonin metabolism, suggesting the development of tolerance initiated by the lower dose. After 7 days exposure to 0.7 ppm ozone, lung ventilatory function measurements revealed small though significant decreases in several parameters. Electron microscopic evaluation of lung capillary endothelium from animals exposed to the 0.7 ppm ozone showed no changes. Positive control animals exposed to greater than 95% oxygen, 20 hr/day for 2 days showed a 23% decrease in serotonin removal (p less than 0.03) and a 12% decrease in HHL removal (p less than 0.017). These studies indicate that inhalation of ozone can induce functional alterations in the lung endothelium, and that this effect occurs at a dosage of ozone that produces minimal ventilatory changes and no observable endothelial ultrastructural changes.

摘要

本研究的主要目的是确定吸入臭氧对肺血管内皮的影响。将雄性Fischer-344大鼠暴露于0.5或0.7 ppm的臭氧中,每天20小时,持续7天。切除肺脏并用含有[14C]血清素或[14C]马尿酸组氨酸亮氨酸(HHL)的 Krebs 培养基进行灌注。与对照组相比,暴露于较低臭氧浓度的动物在血清素清除方面没有统计学上的显著变化。相反,较高的臭氧浓度导致血清素清除率降低32%(p<0.0001),但对HHL没有影响。同样暴露于0.7 ppm臭氧但在清洁空气中恢复14天的大鼠与对照组相比,血清素清除率没有降低。依次暴露于0.5 ppm臭氧7天然后再暴露于0.7 ppm臭氧7天的动物,其血清素代谢没有改变,这表明低剂量引发了耐受性的发展。暴露于0.7 ppm臭氧7天后,肺通气功能测量显示几个参数虽有小幅但显著的下降。对暴露于0.7 ppm臭氧的动物的肺毛细血管内皮进行电子显微镜评估,未发现变化。暴露于大于95%氧气、每天20小时、持续2天的阳性对照动物,血清素清除率降低23%(p<0.03),HHL清除率降低12%(p<0.017)。这些研究表明,吸入臭氧可诱导肺内皮的功能改变,并且这种效应发生在产生最小通气变化且无明显内皮超微结构变化的臭氧剂量下。

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