Ono Koichi, Koizumi Tomonobu, Tsushima Kenji, Yoshikawa Sumiko, Yokoyama Toshiki, Nakagawa Rikimaru, Obata Toru
Department of Anesthesiology and Resuscitation, Shinshu University School of Medicine, Matsumoto, Japan.
Biochem Biophys Res Commun. 2009 Oct 16;388(2):297-300. doi: 10.1016/j.bbrc.2009.07.157. Epub 2009 Aug 5.
The present study was performed to examine a role of oxidative stress in oleic acid-induced lung injury model. Fifteen anesthetized sheep were ventilated and instrumented with a lung lymph fistula and vascular catheters for blood gas analysis and measurement of isoprostanes (8-epi prostaglandin F2alpha). Following stable baseline measurements, oleic acid (0.08 ml/kg) was administered and observed 4 h. Isoprostane was measured by gas chromatography mass spectrometry with the isotope dilution method. Isoprostane levels in plasma and lung lymph were significantly increased 2 h after oleic acid administration and then decreased at 4 h. The percent increases in isoprostane levels in plasma and lung lymph at 2 h were significantly correlated with deteriorated oxygenation at the same time point, respectively. These findings suggest that oxidative stress is involved in the pathogenesis of the pulmonary fat embolism-induced acute lung injury model in sheep and that the increase relates with the deteriorated oxygenation.
本研究旨在探讨氧化应激在油酸诱导的肺损伤模型中的作用。对15只麻醉的绵羊进行通气，并安装肺淋巴瘘管和血管导管，用于血气分析和异前列腺素（8-表前列腺素F2α）的测量。在稳定的基线测量后，给予油酸（0.08 ml/kg）并观察4小时。采用同位素稀释法通过气相色谱-质谱联用仪测定异前列腺素。油酸给药后2小时，血浆和肺淋巴中的异前列腺素水平显著升高，然后在4小时时下降。血浆和肺淋巴中异前列腺素水平在2小时时的升高百分比分别与同一时间点的氧合恶化显著相关。这些发现表明，氧化应激参与了绵羊肺脂肪栓塞诱导的急性肺损伤模型的发病机制，且这种升高与氧合恶化有关。
