Effects of propofol on gastric mucosal cellular apoptosis after resuscitation of hemorrhagic shock in rabbits
10.3760/cma.j.issn.0254-1416.2012.04.027
- VernacularTitle:异丙酚对失血性休克/复苏兔胃黏膜细胞凋亡的影响
- Author:
Lifeng ZHANG
;
Yanxia Lü
;
Haiying LI
;
Qiujun WANG
- Publication Type:Journal Article
- Keywords:
Propofol;
Shock,hemorrhagic;
Resuscitation;
Gastric mucosa;
Apoptosis
- From:
Chinese Journal of Anesthesiology
2012;32(4):488-490
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of propofol on gastric mucosal cellular apoptosis after resuscitation of hemorrhagic shock in rabbits.Methods One hundred healthy adult male New Zealand rabbits weighing 2.5-3.0 kg were randomly divided into 5 groups ( n =20 each):group sham operation (group S) ; group hemorrhagic shock ( group M ) and Ⅲ,Ⅳ,Ⅴ 3 propofol groups ( groups P1,2,3 ).Hemorrhagic shock was induced by withdrawing blood from femoral artery.MAP was reduced to 35-40 mm Hg and maintained at this level for 60 min in groups M,P1,P2 and P3.Blood was then transfused back via femoral vein to restore blood volume.In groups P1,2,3 propofol 5 mg/kg was injectel iv at 10 min before ischemia (group P1 ),10 min before (group P2 ) and 20 min of resuscitation (group P3 ) respectively followed by continuous infusion at 20 mg·kg-1 ·h-1 until 90 min of resuscitation.The gastric mucous membrane specimens were obtained at 90 min of resuscitation for macroscopic examination and detection of apoptosis (by TUNEL) and Bcl-2 and Bax protein expression (by immuno-histochemistry).Results Hemorrhagic shock seriously damaged gastric mucous membrane,significantly increased apoptotic index (the number of apoptotic cells/the total number of cells) and Bax protein expression and decreased Bcl-2 protein expression and Bcl-2/Bax ratio in group M as compared with group S.Propofol significantly attenuated hemorragic shock-induced above changes in groups P1 and P2.Concluion Pre- and post-conditioning with propofol can attenuate apoptosis in gastric mucous membrane cells induced by hemorrhagic shock by up-regulating Bcl-2 protein expression and down-regulating Bax protein expression.
