Effect of cyclooxygenase-2 inhibitor pretreatment on gas exchange after hydrochloric acid aspiration in rats
Effect of cyclooxygenase-2 inhibitor pretreatment on gas exchange after hydrochloric acid aspiration in rats
复制标题
DOI：
10.1007/s00540-005-0322-4
复制
发表时间：
2005-08
影响因子：
2.8
通讯作者：
Y. Terao;Toshiaki Nakamura;H. Morooka;K. Sumikawa
中科院分区：
文献类型：
--
作者：
Y. Terao;Toshiaki Nakamura;H. Morooka;K. Sumikawa
本研究旨在观察环氧化酶-2（考克斯-2）抑制剂对大鼠酸吸入性肺损伤的影响。将大鼠分为四组。H组行盐酸腔内滴注。S组行生理盐水灌胃。HC组于腹腔内注入盐酸前30 min静脉注射考克斯-2抑制剂塞来昔布10 mg/kg。C组仅行支气管肺泡灌洗（BAL）。所有大鼠在BAL前机械通气30 min。BAL前即刻进行动脉血气分析。将H、S和HC组再分为两组。H-1、S-1和HC-1组在滴注后1 h接受BAL，而H-8、S-8和HC-8组在滴注后8 h接受BAL。用支气管肺泡灌洗液测定前列腺素E2（PGE 2）浓度。肠内盐酸导致氧合受损。考克斯-2抑制剂滴注后8 h可减轻氧合损伤，但1 h后无明显变化。肠内盐酸可引起前列腺素E_2浓度升高。考克斯-2抑制剂在滴注后8 h可减弱PGE 2浓度的升高，但在1 h后则无此作用。结果表明，考克斯-2抑制剂可减轻酸吸入性肺损伤大鼠炎症期氧合损伤和肺泡PGE 2浓度升高。
The present study was carried out to determine the effect of cyclooxygenase-2 (COX-2) inhibitor on acid aspiration-induced lung injury in rats. Rats were allocated into one of four groups. Group H received intratracheal instillation of HCl. Group S received saline intratracheally. Group HC received COX-2 inhibitor (celecoxib) 10 mg/kg intravenously 30 min before intratracheal instillation of HCl. Group C underwent bronchoalveolar lavage (BAL) only. All rats were mechanically ventilated for 30 min before BAL. Arterial blood gas analysis was done immediately before BAL. Groups H, S, and HC were subdivided to each two groups. Groups H-1, S-1, and HC-1 underwent BAL 1 h after instillation, whereas groups H-8, S-8, and HC-8 underwent BAL 8 h after instillation. The BAL fluid was used to measure the prostaglandin E2(PGE2) concentration. Intratracheal HCl resulted in impaired oxygenation. COX-2 inhibitor attenuated the impairment of oxygenation 8 h after instillation but not after 1 h. Intratracheal HCl caused an increase in PGE2concentration. COX-2 inhibitor attenuated an increase in PGE2concentration 8 h after instillation but not after 1 h. The results show that COX-2 inhibitor attenuates the oxygenation impairment and the increase in alveolar PGE2 concentration during the inflammatory phase of acid aspiration-induced lung injury in rats.