Effect of penehyclidine hydrochloride pretreatment on activity of NF-κB in lung tissue following acute lung injury induced by hemorrhagic shock in rats
10.3760/cma.j.issn.0254-1416.2010.04.034
- VernacularTitle:盐酸戊乙奎醚预先给药对失血性休克大鼠急性肺损伤时NF-κB活性的影响
- Author:
Dixin WANG
;
Ling DAN
- Publication Type:Journal Article
- Keywords:
Cholinergic antagonists;
Shock,hemorrhagic;
Respiratory distress syndrome,adult;
NF-kappa B
- From:
Chinese Journal of Anesthesiology
2010;30(4):497-499
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of pretreatment with penehychidine hydrochloride(PHCD) on NF-κB activity in the lung tissue following acute lung injury(ALI)induced by hemorrhagic shock in rats.Methods Twenty-four Wistar rats of both sexes weighing 200-250 g were randomly divided into 3 groups (n=8 each):group Ⅰ sham operation (group S);group Ⅱ ALI and group Ⅲ PHCD.The animals were anesthetized with intraperitoneal chloral hydrate 350 mg/kg.Hemorrhagic shock was produced in group Ⅱ and Ⅲ.Right carotid artery was cannulated for BP monitoring.Left femoral artery was cannulated for blood letting.MAP was reduced to 35-45 mm Hg within 10 min and maintained for 1 h in group ALI and PHCD(group Ⅱ andⅢ).The animals were then resuscitated with blood and normal saline.PHCD 2 mg/kg was given iv immediately before blood-letting in group PHCD.Blood samples were obtained from artery at 6 h after hemorrhagic shock wag induced for blood gas analysis and from right auricle for determination of plasma TNF-α concentration by ELISA.The lungs were then harvested for microscopic examination and determination of the expression of NF-κB p65 by immuno-histochemistry and W/D lung weight ratio.Results The plasma TNF-α concentration and expression of NF-κB p65 in the lung tissue were significantly increased in group ALI and PHCD as compared with group S and were significantly lower in group PHCD than in group ALI.There was less damage to the lung tissue in group PHCD than in group ALI.Conclusion PHCD pretreatment can attenuate ALl induced by hemorrhagic shock by inhibiting NF-κB activity.
