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大鼠不完全性脑缺血后右美托咪定和低温联合的神经保护作用。

Neuroprotective effects of a combination of dexmedetomidine and hypothermia after incomplete cerebral ischemia in rats.

机构信息

Department of Anesthesia and Intensive Care Medicine, Akita University School of Medicine, Akita 010-8543, Japan.

出版信息

Acta Anaesthesiol Scand. 2010 Mar;54(3):377-82. doi: 10.1111/j.1399-6576.2009.02139.x. Epub 2009 Oct 26.

DOI:10.1111/j.1399-6576.2009.02139.x
PMID:19860751
Abstract

BACKGROUND

Dexmedetomidine and hypothermia are known to reduce neuronal injury following cerebral ischemia. We examined whether a combination of dexmedetomidine and hypothermia reduces brain injury after transient forebrain ischemia in rats to a greater extent than either treatment alone.

METHODS

Thirty-eight male Sprague-Dawley rats were anesthetized with fentanyl and nitrous oxide in oxygen. Four groups were tested: group C (saline 1 ml/kg, temporal muscle temperature 37.5 degrees C); group H (saline 1 ml/kg, 35.0 degrees C); group D (dexmedetomidine 100 microg/kg, 37.5 degrees C); and group DH (dexmedetomidine 100 microg/kg, 35.0 degrees C). Dexmedetomidine or saline was administered intraperitoneally 30 min before ischemia. Cerebral ischemia was produced by right carotid artery ligation with hemorrhagic hypotension (mean arterial pressure 40 mmHg) for 20 min. Neurologic outcome was evaluated at 24, 48, and 72 h after ischemia. Histopathology was evaluated in the caudate and hippocampus at 72 h after ischemia.

RESULTS

Neurologic outcome was significantly better in the group DH than the group C (P<0.05), whereas it was similar between the group DH and the groups D or H. Survival rate of the hippocampal CA1 neurons was significantly greater in groups D, H, and DH than group C (P<0.05). Histopathologic injury in the caudate section was significantly less in groups H and DH than group C (P<0.05).

CONCLUSION

The combination of dexmedetomidine and hypothermia improved short-term neurologic outcome compared with the control group, whereas the combination therapy provided comparable neuroprotection with either of the two therapies alone.

摘要

背景

右美托咪定和低温已知可减少脑缺血后的神经元损伤。我们研究了右美托咪定和低温联合应用是否比单独应用更能减轻大鼠短暂性前脑缺血后的脑损伤。

方法

38 只雄性 Sprague-Dawley 大鼠在氧气中的芬太尼和一氧化二氮麻醉下。测试了四组:组 C(生理盐水 1ml/kg,颞肌温度 37.5°C);组 H(生理盐水 1ml/kg,35.0°C);组 D(右美托咪定 100μg/kg,37.5°C);组 DH(右美托咪定 100μg/kg,35.0°C)。右美托咪定或生理盐水在缺血前 30 分钟腹腔内给药。通过右颈总动脉结扎和出血性低血压(平均动脉压 40mmHg)产生脑缺血 20 分钟。缺血后 24、48 和 72 小时评估神经功能结局。缺血后 72 小时评估尾状核和海马的组织病理学。

结果

组 DH 的神经功能结局明显优于组 C(P<0.05),而组 DH 与组 D 或组 H 之间相似。组 D、H 和 DH 的海马 CA1 神经元存活率明显高于组 C(P<0.05)。尾状核切片的组织病理学损伤在组 H 和 DH 明显小于组 C(P<0.05)。

结论

与对照组相比,右美托咪定和低温联合治疗可改善短期神经功能结局,而联合治疗与两种治疗单独应用相比提供了相当的神经保护作用。

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