Bederson J B, Levy A L, Ding W H, Kahn R, DiPerna C A, Jenkins A L, Vallabhajosyula P
Department of Neurosurgery, Mount Sinai School of Medicine, New York, New York 10029-6574, USA.
Neurosurgery. 1998 Feb;42(2):352-60; discussion 360-2. doi: 10.1097/00006123-199802000-00091.
Decreased cerebral blood flow (CBF) and cerebral ischemia occurring immediately after subarachnoid hemorrhage (SAH) may be caused by acute microvascular constriction. However, CBF 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.
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.
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.
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.
蛛网膜下腔出血（SAH）后立即出现的脑血流量（CBF）降低和脑缺血可能是由急性微血管收缩所致。然而，CBF也可受颅内压（ICP）和脑灌注压（CPP）变化的影响。这些实验的目的是评估SAH后急性血管收缩的意义及其与CBF、ICP、CPP和细胞外谷氨酸浓度变化的关系。
采用血管内丝线技术进行三项实验以造成SAH。在第一个实验中，在SAH后60分钟测量CBF、ICP和CPP（n = 21），并将其与24小时死亡率相关联。在第二个实验中，对接受SAH的大鼠（n = 23）或假手术的大鼠（n = 7）在SAH后60分钟进行灌注，以测量颈内动脉和大脑前动脉的周长和壁厚，并将其与CBF、ICP和CPP相关联。在第三个实验（n = 11）中，通过海马和皮质微透析及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联。
SAH后60分钟CBF降低至低于基线的40%可100%准确预测24小时死亡率，并用于定义“致死性”SAH。相比之下，SAH后60分钟的ICP和CPP与死亡率无关。致死性SAH组的血管周长明显小于非致死性SAH组或假手术大鼠（P < 0.001）。血管测量值与CBF和出血大小均相关（P < 0.01）。致死性SAH后海马和皮质的细胞外谷氨酸浓度均增加至基线的600%，且与CBF呈负相关（r = 0.9，P < 0.001），而非致死性SAH后未增加。
SAH后的急性血管收缩独立于ICP和CPP的变化而发生，且与CBF降低、出血量大、细胞外谷氨酸持续升高及预后不良相关。急性血管收缩似乎直接导致SAH后的缺血性脑损伤。对具有逆转急性血管收缩潜力的药物进行进一步评估可能会增加CBF并改善预后。
