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实验性脑血管痉挛中脑池内与颈内动脉内输注L-精氨酸的比较

Intracisternal versus intracarotid infusion of L-arginine in experimental cerebral vasospasm.

作者信息

Ozüm Unal, Aslan Adem, Karadağ Ozen, Gürelik Mustafa, Taş Ayşenur, Zafer Kars H

机构信息

Department of Neurosurgery, Cumhuriyet University Faculty of Medicine, Sivas, Turkey.

出版信息

J Clin Neurosci. 2007 Jun;14(6):556-62. doi: 10.1016/j.jocn.2006.03.013.

Abstract

AIM

The effect of short term intracisternal and intracarotid L-arginine infusion on experimental cerebral acute phase vasospasm in a rabbit subarachnoid haemorrhage model is investigated, and the two groups compared.

MATERIALS AND METHOD

Subarachnoid haemorrhage was produced by intracisternal injection of autologous blood in New Zealand rabbits. On the fourth day after subarachnoid haemorrhage, cerebral blood flow was monitored using transcranial Doppler ultrasonography during intracisternal and intracarotid saline and L-arginine infusions.

RESULT

Cerebral blood flow measurements revealed resolution of vasospasm with short-term intracisternal and intracarotid L-arginine infusion. No significant difference was found between the effects of intracisternal and intracarotid L-arginine infusions, however intracarotid L-arginine infusion created a more potent vasodilatation towards the end of infusion.

CONCLUSION

Both intracisternal and intracarotid short term L-arginine infusion significantly improve acute phase cerebral vasospasm after experimental subarachnoid haemorrhage. Intracarotid L-arginine infusion is more potent and safer as large amounts of intracisternal L-arginine may lead to overproduction of nitric oxide by inducible nitric oxide synthase with the production of free radicals.

摘要

目的

研究新西兰兔蛛网膜下腔出血模型中,短期脑池内和颈内动脉注射L-精氨酸对实验性脑急性期血管痉挛的影响,并对两组进行比较。

材料与方法

通过向新西兰兔脑池内注射自体血来制造蛛网膜下腔出血。蛛网膜下腔出血后第4天,在脑池内和颈内动脉注射生理盐水及L-精氨酸期间,使用经颅多普勒超声监测脑血流量。

结果

脑血流量测量显示,短期脑池内和颈内动脉注射L-精氨酸可缓解血管痉挛。脑池内和颈内动脉注射L-精氨酸的效果之间未发现显著差异,然而颈内动脉注射L-精氨酸在输注结束时产生了更强的血管扩张作用。

结论

脑池内和颈内动脉短期注射L-精氨酸均可显著改善实验性蛛网膜下腔出血后的急性期脑血管痉挛。颈内动脉注射L-精氨酸更有效且更安全,因为大量脑池内注射L-精氨酸可能导致诱导型一氧化氮合酶过度产生一氧化氮并产生自由基。

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