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果糖-1,6-二磷酸可减少大鼠大脑中动脉可逆性闭塞后的梗死体积。

Fructose-1,6-bisphosphate reduces infarct volume after reversible middle cerebral artery occlusion in rats.

作者信息

Kuluz J W, Gregory G A, Han Y, Dietrich W D, Schleien C L

机构信息

Department of Pediatrics, University of Miami, School of Medicine, FL 33101.

出版信息

Stroke. 1993 Oct;24(10):1576-83. doi: 10.1161/01.str.24.10.1576.

DOI:10.1161/01.str.24.10.1576
PMID:8378964
Abstract

BACKGROUND AND PURPOSE

We tested the hypothesis that fructose-1,6-bisphosphate, when administered 10 minutes before the end of 2 hours of reversible middle cerebral artery occlusion, reduces ischemia-reperfusion injury and infarct volume measured after a 3-day survival period in rats.

METHODS

After 1 hour and 50 minutes of middle cerebral artery occlusion by the intraluminal suture method, fructose-1,6-bisphosphate, 500 mg/kg in group 1 and 350 mg/kg in group 2 (or an equivalent volume of 1.8% saline as placebo in each group), was given intravenously for a period of 15 minutes to fasted adult Sprague-Dawley rats. After 2 hours of ischemia, the suture was withdrawn and the rats allowed to survive for 3 days. The areas of infarction in 10 hematoxylin-eosin-stained coronal sections of the brain were measured and used to calculate infarct volume.

RESULTS

In group 1, fructose-1,6-bisphosphate decreased total cerebral hemispheric infarct volume by 43% (from 199.6 +/- 11.2 to 114.2 +/- 35.8 mm3, P < .04; mean +/- SEM). Cerebral cortical and subcortical infarct volumes were decreased by 46% (from 137.3 +/- 7.5 to 74.1 +/- 28.6 mm3, P < .04) and 36% (from 62.3 +/- 5.1 to 40.0 +/- 8.3 mm3, P < .04), respectively. In group 2, fructose-1,6-bisphosphate had no effect on infarct volume in rats that developed mild intraischemic hyperthermia, but in rats kept normothermic during ischemia, fructose-1,6-bisphosphate reduced subcortical infarct volume from 53.7 +/- 8.1 to 18.4 +/- 8.0 mm3 (P < .03).

CONCLUSIONS

Fructose-1,6-bisphosphate improves functional neurological outcome and reduces infarct volume after reversible middle cerebral artery occlusion in rats.

摘要

背景与目的

我们检验了如下假设:在大脑中动脉可逆性闭塞2小时结束前10分钟给予1,6-二磷酸果糖,可减少大鼠生存3天后测得的缺血再灌注损伤和梗死体积。

方法

采用管腔内缝合方法使大脑中动脉闭塞1小时50分钟后,分别给予成年禁食斯普拉格-道利大鼠静脉注射1,6-二磷酸果糖,第1组剂量为500mg/kg,第2组为350mg/kg(或每组给予等量的1.8%盐水作为安慰剂),持续15分钟。缺血2小时后,拔出缝合线,让大鼠存活3天。测量10张苏木精-伊红染色的大脑冠状切片的梗死面积,用于计算梗死体积。

结果

在第1组中,1,6-二磷酸果糖使大脑半球总梗死体积减少43%(从199.6±11.2降至114.2±35.8mm3,P<.04;均值±标准误)。大脑皮质和皮质下梗死体积分别减少46%(从137.3±7.5降至74.1±28.6mm3,P<.04)和36%(从62.3±5.1降至40.0±8.3mm3,P<.04)。在第2组中,1,6-二磷酸果糖对发生轻度缺血性体温过高的大鼠的梗死体积没有影响,但在缺血期间保持正常体温的大鼠中,1,6-二磷酸果糖使皮质下梗死体积从53.7±8.1降至18.4±8.0mm3(P<.03)。

结论

1,6-二磷酸果糖可改善大鼠大脑中动脉可逆性闭塞后的神经功能结局并减少梗死体积。

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