Effects of postconditioning with leg ischemia on focal cerebral ischemia-reperfusion injury in diabetic rats
10.3760/cma.j.issn.0254-1416.2009.01.015
- VernacularTitle:肢体缺血后处理对糖尿病大鼠局灶性脑缺血再灌注损伤的影响
- Author:
Yan LI
;
Cuilan WANG
;
Yingyun LU
- Publication Type:Journal Article
- Keywords:
Lower extremity;
Reperfusion injury;
Brain;
Diabetes mellitus;
lscbemic postconditioning
- From:
Chinese Journal of Anesthesiology
2009;29(1):50-52
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effects of leg ischemic postconditioning on focal cerebral ischemia-reperfusion (I/R) injury in diabetic rats. Methods Forty male diabetic SD rats weighing 270-320 g were randomly assigned to one of 4 groups (n=10 each):group Ⅰcontrol (C);group Ⅱ sham operation (S);group Ⅲ fecal cerebral ischemia-repertusion (I/R) and group Ⅳ leg ischemic postconditioning (IPC). Diabetes mellitus was induced by intraperitoneal streptozotocin. Local cerebral I/R was produced by middle cerebral artery occlusion (MCAO) for 1.5 h followed by 6 h reperfusion. A nylon thread with rounded tip was inserted into internal carotid artery and threaded cranially until resistance was felt. Leg isebemia was induced by placing tourniquet on beth legs at 30 min before repeffusion. The animals underwent 3 episodes of 5 min leg ischemia at 5 min intervals. Neuro-functional deficit was assessed and recorded at the end of 6h reperfusion using neurologic deficit scores (NDS) (0=no deficit, 4=unable to crawl and semiconscious). The animals were then decapitated and their brains were removed for determination of volume of cerebral infaret (by TIC staining) and ratio' of neuronal apoptosis (by TUNEL). Results NDS and cerebral infarct volume were significantly increased at the end of 6 h reperfusion in group I/R and IPC as compared with group C and S. IPC significantly decreased cerebral infarct volume and ratio of neuronal apoptosis induced by MCAO. There was no significant difference in NDA between group I/R and IPC. Conclusion Leg iscbemic postconditioning can protect the brain against focal cerebral I/R injury in diabetic rats.
