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重度创伤性脑损伤后脑血管中L-精氨酸的反应性

L-arginine reactivity in cerebral vessels after severe traumatic brain injury.

作者信息

Rangel-Castilla Leonardo, Ahmed Osama, Goodman J Clay, Gopinath Shankar, Valadka Alex, Robertson Claudia

机构信息

Department of Neurosurgery, The Methodist Neurological Institute, The Methodist Hospital, Houston, TX, USA.

出版信息

Neurol Res. 2010 Dec;32(10):1033-40. doi: 10.1179/016164110X12767786356598. Epub 2010 Aug 16.

DOI:10.1179/016164110X12767786356598
PMID:20712924
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2958228/
Abstract

OBJECTIVES

Traumatic brain injury (TBI) causes an early reduction of cerebral blood flow (CBF). The purpose was to study cerebrovascular endothelial function by examining the reactivity of cerebral vessels to L-arginine.

METHODS

Fifty-one patients with severe TBI were prospectively studied by measuring cerebral hemodynamics before and after the administration of L-arginine, 300 mg/kg at 12 hours and at 48 hours after injury. These hemodynamic measurements, using transcranial Doppler techniques, included internal carotid flow volume as an estimate of hemispheric CBF, flow velocity in intracranial vessels, CO(2) reactivity, and dynamic pressure autoregulation using thigh cuff deflation and carotid compression methods. Changes in the hemodynamics with L-arginine administration were analyzed using a general linear mixed model.

RESULTS

L-arginine produced no change in mean arterial pressure, intracranial pressure, or brain oxygenation. Overall, L-arginine induced an 11.3% increase in internal carotid artery flow volume (P=0.0190). This increase was larger at 48 hours than at 12 hours (P=0.0045), and tended to be larger in the less injured hemisphere at both time periods. The response of flow velocity in the intracranial vessels was similar, but smaller differences with administration of L-arginine were observed. There was a significant improvement in CO(2) reactivity with L-arginine, but no change in dynamic pressure autoregulation.

DISCUSSION

The low response of the cerebral vessels to L-arginine at 12 hours post-injury with improvement at 48 hours suggests that dysfunction of cerebrovascular endothelium plays a role in the reduced CBF observed after TBI.

摘要

目的

创伤性脑损伤(TBI)会导致脑血流量(CBF)早期减少。本研究旨在通过检测脑血管对L-精氨酸的反应性来研究脑血管内皮功能。

方法

前瞻性研究51例重度TBI患者,在伤后12小时和48小时给予300mg/kg L-精氨酸,测量给药前后的脑血流动力学。这些血流动力学测量采用经颅多普勒技术,包括将颈内动脉血流量作为半球CBF的估计值、颅内血管流速、CO₂反应性以及使用大腿袖带放气和颈动脉压迫方法进行的动态压力自动调节。使用一般线性混合模型分析给予L-精氨酸后血流动力学的变化。

结果

L-精氨酸对平均动脉压、颅内压或脑氧合无影响。总体而言,L-精氨酸使颈内动脉血流量增加了11.3%(P=0.0190)。48小时时的增加幅度大于12小时时(P=0.0045),并且在两个时间段内,损伤较轻的半球增加幅度往往更大。颅内血管流速的反应相似,但与给予L-精氨酸的差异较小。L-精氨酸使CO₂反应性有显著改善,但动态压力自动调节无变化。

讨论

伤后12小时脑血管对L-精氨酸反应低,48小时有所改善,这表明脑血管内皮功能障碍在TBI后观察到的CBF减少中起作用。

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Statin treatment improves cerebral more than systemic endothelial dysfunction in patients with arterial hypertension.他汀类药物治疗对高血压患者脑内皮功能障碍的改善作用大于全身内皮功能障碍。
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