| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
From the *Department of Anesthesiology, the First Affiliated Hospital, School of Medicine, Zhejiang University, People’s Republic of China; and Department of Pharmacology, School of Medicine, Zhejiang University, Hang Zhou, People’s Republic of China.
Address correspondence and reprint requests to Sheng-Mei Zhu, MD, PhD, Department of Anesthesiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qingchun Road, 310003, HangZhou, People’s Republic of China. Address e-mail to smzhu20088{at}yahoo.com.cn.
Abstract
BACKGROUND: Cerebral edema is a major threat for stroke victims. Most studies have focused on the neuroprotective activities of propofol, addressing infarct volume rather than cerebral edema. Aquaporin-4 (AQP4) plays an important role in maintaining brain water homeostasis under various neurological insults. We explored the effect of propofol pretreatment on cerebral edema in a rat model of brain ischemia reperfusion and assessed the involvement of AQP4.
METHODS: To induce brain ischemia reperfusion, we introduced a silicone-coated monofilament nylon suture into the origin of the middle cerebral artery, withdrawing it after 90 min. Treatment groups (n = 32), received propofol (0.1 mL · kg–1 · min–1) infusion for 30 min before occlusion; the vehicle group (n = 32) and the sham-operated group (n = 28), which received the intralipid vehicle at the same time and rate. To assess cerebral infarct volume, we used 2, 3, 5-triphenyl-tetrazolium chloride staining; wet–dry weight ratio was the basis for cerebral edema estimation, and we used immunohistochemistry and Western blot to detect AQP4 expression.
RESULTS: The wet–dry weight ratio decreased from 86.89% ± 0.71% in the vehicle group (n = 6) to 72.42% ± 0.74% in the propofol group (n = 6), corresponding to an average decrease of 16%. In parallel and based on immunohistochemical semi-quantification, the propofol group exhibited remarkable attenuation of AQP4 over-expression in the ischemic border zone compared with the vehicle group: 1.28 ± 0.03 vs 1.40 ± 0.05, n = 7, respectively; P < 0.05. Values derived from Western blot quantification were similarly decreased in the propofol group compared to the vehicle group: 20.85% ± 4.18% vs 31.67% ± 3.23%, n = 4, respectively; P < 0.05. However, infarct volume and neurologic deficit in postischemic rats in the propofol group were not statistically different from values in the vehicle group.
CONCLUSIONS: We conclude that prestroke treatment with propofol reduces postischemic cerebral edema in rats, possibly through inhibiting AQP4 over-expression in the boundary zone of ischemia.
This article has been cited by other articles:
|
|
 |
|
  N. Bruder, C. Ichai, and A. W. Gelb Hyponatremia and Subarachnoid Hemorrhage: Will That Be One Pinch or Two of Salt? Anesth. Analg., June 1, 2009; 108(6): 1734 - 1735. [Full Text] [PDF]
|
|
|
