在实验性脑血管痉挛模型中，一氧化氮合酶抑制可减弱对脊髓刺激的血管活性反应。

Nitric oxide synthase inhibition attenuates vasoactive response to spinal cord stimulation in an experimental cerebral vasospasm model.

作者信息

Göksel H M, Karadag O, Turaçlar U, Taş F, Oztoprak I

机构信息

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

出版信息

Acta Neurochir (Wien). 2001;143(4):383-90; discussion 390-1. doi: 10.1007/s007010170094.

DOI:10.1007/s007010170094

PMID:11437293

Abstract

BACKGROUND

The basic mechanism of delayed cerebral vasospasm following subarachnoid haemorrhage (SAH) has been intensively investigated. It is thought that nitric oxide (NO) is a basic mediator of the cerebral vasodilator mechanism. Previous clinical and experimental studies have shown a cerebral vasodilator effect of high cervical spinal cord stimulation (SCS) however, the mechanism of this effect is still controversial. We investigated the contribution of the vasodilator effect of NO to this mechanism in an experimental SAH model using rabbits.

METHOD

Four experimental groups, were designated: Group 1. Cerebral blood flow (CBF) was evaluated by transcranial Doppler ultrasonography (TDU) in 8 rabbits. Group 2. In 4 animals, intracisternal saline injection and cervical epidural electrode placement without SCS were performed before TDU. Group 3. TDU was performed before and after SCS on the fourth day of SAH in 8 rabbits. Group 4. In 8 animals, N-Nitro-L-Arginine Methyl Esther (L-NAME) was administered intracisternally on the fourth day of SAH, at a dose of 0.6 mg/kg, 45 minutes before SCS. CBF parameters, obtained via measurements or calculations from TDU data, were compared.

FINDINGS

The occurrence of vasospasm after SAH was demonstrated with significant changes in TDU parameters (high peak systolic velocity and positive values of the degree of stenosis). In all SAH animals, SCS resulted in significant vasodilation. Even after the injection of L-NAME, SCS still had a significant vasodilatory effect in SAH animals, but there was also a significant difference in CBF parameters in the SCS-only group when compared with the L-NAME treatment before SCS group.

INTERPRETATION

The mechanism of the cerebral vasodilatory effect of SCS remains controversial. Our results revealed the contribution of a neurohumoral effect which can be partially prevented by use of an NO synthase inhibitor.

摘要

背景

蛛网膜下腔出血（SAH）后迟发性脑血管痉挛的基本机制已得到深入研究。一氧化氮（NO）被认为是脑血管舒张机制的基本介质。先前的临床和实验研究表明，高颈段脊髓刺激（SCS）具有脑血管舒张作用，然而，这种作用的机制仍存在争议。我们在兔实验性SAH模型中研究了NO的血管舒张作用对该机制的贡献。

方法

设立四个实验组：第1组。通过经颅多普勒超声（TDU）评估8只兔的脑血流量（CBF）。第2组。在4只动物中，于TDU检查前进行脑池内盐水注射和颈段硬膜外电极置入但不进行SCS。第3组。在8只兔SAH后第4天，于SCS前后进行TDU检查。第4组。在8只动物中，于SAH后第4天，在SCS前45分钟，脑池内给予N-硝基-L-精氨酸甲酯（L-NAME），剂量为0.6 mg/kg。比较通过TDU数据测量或计算获得的CBF参数。