Effects of isoflurane inhalation during reperfusion on different degrees of global cerebral ischemiareperfusion injury in rats
- VernacularTitle:再灌注期吸入异氟醚对不同程度大鼠脑缺血再灌注损伤的影响
- Author:
Yong-Hai SUN
;
Yun YUE
;
Yun WANG
;
- Publication Type:Journal Article
- Keywords:
Isoflurane;
Brain ischemia;
Reperfusion injury;
Excitatory amino acids;
Apoptosis
- From:
Chinese Journal of Anesthesiology
1995;0(12):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective Isoflurane preconditioning has been shown to protect against cerebral ischemia-reperfusion(I/R)injury.The purpose of this study was to investigate if isoflurane inhalation during reperfusion hasany protective effects.Methods Fourty-two SD rats weighing 318-365 g were randomly divided into 3 groups:sham group(n=6),control group(n=18)and isoflurane group(n=18).Control group and isoflurane groupwere further divided into 10,15 and 20 rain ischernia subgroups(subgroup A,B,C,n=6).In isoflurane group1.4% isoflurane in air was inhaled immediately after reperfusion was started for 30 min.Two days before theexperiment the animals were anesthetized with intraperitoneal chloral hydrate 300 mg?kg~(-1).Microdialysis catheterwas inserter into right hippocampns using stereotactic technique and fixed.BIS microelectrodes were placed in thebrain.Vertebral arteries were permanendy occluded by electric coagulation.Bilateral common carotid arteries wereexposed and atranmatic sutures were placed around them.Globol cerebral ischemia was produced by tighteningcarotid sutures and maintained for 10,15 or 20 min(subgroup A,B,C).Cerebral iscbemia was confirmed by lossof righting reflex,dilated pupils,loss of light reflex,BIS=0 and isoelectric potential on EEG.Carotid sutureswere then released for reperfusion.Isoflurane inhalation was started right after the beginning of reperfusion andmaintained for 30 min.Neurologlc outcome was assessed by motor performance according to Combs(0-10,0=severe dysfunction,10=no dysfunction)at 24 h,48 h and 72 h of reperfusion.Microdialysis samples werecollected before during and 0-15,15-30,30-45 and 45-60 min after ischemia for determination of glutamateconcentration.Three days after ischemia the animals were sacrificed and brains were removed for microscopicexamination of hippocampns CA1 region.The number of apoptotic(TUNEL positive)neurons were counted and thepercentage(the number of TUNEL positive neurons/the total number of neurons)was calculated.Results Theglutamate content in hippocampus was significantly lower in isoflurane group than in control group duringreperfusion(P
