Acute vasoconstriction after subarachnoid hemorrhage
Acute vasoconstriction after subarachnoid hemorrhage
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DOI：
10.1097/00006123-199802000-00091
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发表时间：
1998-02-01
期刊：
影响因子：
4.8
通讯作者：
Vallabhajosyula, P
中科院分区：
文献类型：
--
作者：
Bederson, JB;Levy, AL;Vallabhajosyula, P
目的：蛛网膜下腔出血(SAH)后即刻发生的脑血流量(CBF)减少和脑缺血可由急性微血管收缩引起，而CEF：也可受颅内压(ICP)和脑灌注压(CPP)的影响。这些实验的目的是评估SAH后急性血管收缩的意义及其与脑血流、颅内压、CPP和细胞外谷氨酸浓度变化的关系。方法：采用血管内细丝技术制作SAH模型。在第一个实验中，测定SAH后60分钟的脑血流量、颅内压和CPP(n=21)，并与24小时死亡率进行相关分析。在实验2中，SAH组(n=23)和假手术组(n=7)在SAH后60min灌流，测量颈内动脉和大脑前动脉的管径和管壁厚度，并与脑血流量、颅内压和CPP进行相关性分析。在第三个实验中(n=11)，通过海马区和皮质微渗析和高效液相色谱法测定的细胞外谷氨酸浓度与生理变化相关。结果：SAH后60min脑血流量下降到基线的40%以下，预测24小时死亡率的准确率为100%，并被用来定义“致死性”SAH。相反，蛛网膜下腔出血后60min的颅内压和CPP与死亡率无关，致死组的血管周径明显小于亚致死组和假手术组(P<；0.001)。血管测量与脑血流量和出血大小相关(P<；0.01)。致死性蛛网膜下腔出血后，海马区和大脑皮层细胞外谷氨酸浓度均升高至基线的600%，并与脑血流量呈负相关(r=0.90，P&0.001)，但亚致死性蛛网膜下腔出血后未见明显升高。结论：蛛网膜下腔出血后急性血管收缩与脑血流量减少、出血范围扩大、细胞外谷氨酸持续升高及不良预后无关。急性血管收缩似乎直接导致SAH后的缺血性脑损伤。进一步评估有可能逆转急性血管收缩的药物可能会增加脑血流量并改善预后。
OBJECTIVE: Decreased cerebral blood flow (CBF) and cerebral ischemia occurring immediately after subarachnoid hemorrhage (SAH) may be caused tay acute microvascular constriction, However, CEF: can also be influenced by changes in intracranial pressure (ICP) and cerebral perfusion pressure (CPP). The goal of these experiments was to assess the significance of acute vasoconstriction after SAH and its relationship to changes in CBF, ICP, CPP, and extracellular glutamate concentrations.METHODS: Three experiments were performed using the endovascular filament technique to produce SAH. In the first experiment, CBF, ICP, and CPP were measured for 60 minutes after SAH (n = 21) and were correlated with the 24-hour mortality rate. in the second experiment, rats undergoing SAH (n = 23) or a sham procedure (n = 7) were perfused 60 minutes after SAH for measurement of the circumference and wall thickness of the internal carotid and anterior cerebral arteries and correlation with CBF, ICP, and CPP. In the third experiment (n = 11), extracellular glutamate concentrations determined by hippocampal and cortical microdialysis and high performance liquid chromatography were correlated with physiological changes.RESULTS: CBF reductions to less than 40% of baseline for 60 minutes after SAH predicted 24-hour mortality with 100% accuracy and were used to define "lethal" SAH. In contrast, ICP and CPP 60 minutes after SAH were not correlated with the mortality rate, The vascular circumference was significantly smaller in lethal than in sublethal SAH or sham-operated rats (P < 0.001). Vessel measurements were correlated with both CBF and hemorrhage size (P < 0.01). Extracellular glutamate concentration increased to 600% of baseline after lethal SAH in both hippocampus and cortex and was inversely correlated with CBF (r = 0.9, P < 0.001) but did not increase after sublethal SAH.CONCLUSION: Acute vasoconstriction after SAH occurs independently of changes in ICP and CPP and is associated with decreased CBF, larger hemorrhage size, persistent elevations of extracellular glutamate, and poor outcome. Acute vasoconstriction seems to contribute directly to ischemic brain injury after SAH. Further evaluations of pharmacological agents with the potential to reverse acute vasoconstriction may increase CBF and improve outcome.