Effect of sevoflurane postconditioning on inositol-requiring enzyme 1 signaling pathway in brain tissues in a rat model of hemorrhagic shock and resuscitation
10.3760/cma.j.issn.0254-1416.2017.06.024
- VernacularTitle:七氟醚后处理对失血性休克复苏大鼠脑组织需肌醇酶1信号通路的影响
- Author:
Qiquan ZHANG
;
Xianwen HU
;
Xiaowen DUAN
;
Jingxian WANG
;
Shufang HE
;
Ye ZHANG
- Keywords:
Protein-serine-threonine kinases;
Anesthetic,inhalation;
Shock,hemorrhagic;
Fluid therapy;
Ischemic postconditioning
- From:
Chinese Journal of Anesthesiology
2017;37(6):731-735
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of sevoflurane postconditioning on inositol-requiring enzyme 1 (IRE1) signaling pathway in the brain tissues in a rat model of hemorrhagic shock and resuscitation (HSR).Methods Sixty healthy adult male Sprague-Dawley rats,weighing 300-350 g,were divided into 5 groups (n =12 each) using a random number table:sham operation group (group Sham),group HSR,1.2％ sevoflurane postconditioning group (group SP1),2.4％ sevoflurane postconditioning group (group SP2) and 3.6％ sevoflurane postconditioning group (group SP3).Hemorrhagic shock was induced by withdrawing blood (40％ of the total blood volume) from the right common carotid artery over an interval of 30 min,and 1 h later the animals were resuscitated with the shed blood infused via the left jugular vein over 30 min.SP1,SP2 and SP3 groups inhaled 1.2％,2.4％ and 3.6％ sevoflurane,respectively,for 30 min starting from the beginning of infusion of the shed blood.Oxygen was inhaled for 30 min instead of sevoflurane in Sham and HSR groups.Mean arterial pressure was recorded before withdrawing blood (T0),immediately after the end of withdrawing blood (T1),at 30 min after the end of withdrawing blood (T2),before infusion of the shed blood (T3),and immediately after infusion of the shed blood (T4).Arterial blood samples were obtained at T0,T1,T3 and T4 for blood gas analysis.Morris water maze test was performed at 72 h after the end of infusion of the shed blood.The animals were then sacrificed,and brains were removed for determination of the expression of caspase-3 in hippocampal CA1 region (by immunohistochemistry) and expression of IRE1 and X-box binding protein 1 (XBP1) in hippocampal tissues (by Western blot).Results Compared with group Sham,mean arterial pressure was significantly decreased at T1-3,the pH value and base excess were decreased,lactic acid concentrations were increased,the escape latency was prolonged,the frequency of crossing the original platform was decreased,and the expression of caspase-3 in hippocampal CA1 regitn and IRE1 and X BP 1 in hippocampal tissues was up-reg ulated in group HSR (P＜0.05).Compared with group HSR,the escape latency was significantly shortened,the frequency of crossing the original platform was increased,and the expression of caspase-3 in hippocampal CA1 region and IRE1 and XBP1 in hippocampal tissues was down-regulated in SP2 and SP3 groups (P＜0.05),and no significant changes were found in the parameters mentioned above in group SP1 (P＞0.05).Conclusion The mechanism by which sevoflurane postconditioning reduces brain injury may be related to activating IRE1 signaling pathway in the brain tissues in a rat model of HSR.
