Clark J F, Pyne G J, Choutka J, Carrozzella J A, Khoury J, Broderick J P, Cadoux-Hudson T A
Department of Neurology, University of Cincinnati, OH, USA.
Acta Neurochir (Wien). 2001;143(7):721-8. doi: 10.1007/s007010170052.
The cerebrospinal fluid (CSF) from subarachnoid haemorrhage (SAH) patients with cerebral vasospasm stimulates vasoconstriction and oxygen consumption in the porcine carotid artery in vitro. Stimulation of oxygen consumption has been used as an in vitro model of vasospasm to assess the relative benefits of nimodipine, isoprenaline, dobutamine, and sodium nitroprusside (SNP).
Samples of human CSF were obtained from SAH patients and applied to de-endothelialised porcine carotid artery. Stimulation of oxygen consumption (as an in vitro marker for a stimulation of the vessels) was monitored and the effects of SNP, isoprenaline, dobutamine or nimodipine were measured.
The CSF from SAH patients with evidence of vasospasm stimulated oxygen consumption to 0.91 +/- 0.17 (microM O2/min/g dry wt, +/- SD p < or = 0.01) and CSF from SAH patients without vasospasm did not significantly stimulate oxygen consumption 0.27 +/- 0.02, with 0.23 +/- 0.03 (microM O2/min/g dry wt) being an unstimulated rate of respiration for the porcine carotid artery. SNP, isoprenaline or dobutamine significantly (p < or = 0.01) decreased the stimulation of oxygen consumption of the porcine carotid artery whereas nimodipine did not. In a cohort of 41 SAH patients who received nimodipine alone or nimodipine and dobutamine, the in hospital mortality rate of the patients who received only nimodipine was 42% as compared to an in hospital mortality rate of 17% in the nimodipine plus dobutamine group P < or = 0.076).
The in vivo data on the 41 patients is not statistically significant, so further studies are required to determine if the differences are important. SNP, isoprenaline and dobutamine significantly decreased oxygen consumption of the porcine carotid arteries exposed to CSF from SAH patients who had vasospasm whereas nimodipine did not. Our in vitro results suggest that these compounds require further study in patients with SAH who are at risk for vasospasm because they may have a direct benefit for the vasospastic arteries.
患有脑血管痉挛的蛛网膜下腔出血（SAH）患者的脑脊液（CSF）在体外可刺激猪颈动脉血管收缩和氧消耗。氧消耗的刺激已被用作血管痉挛的体外模型，以评估尼莫地平、异丙肾上腺素、多巴酚丁胺和硝普钠（SNP）的相对益处。
从SAH患者获取人CSF样本，并应用于去内皮的猪颈动脉。监测氧消耗的刺激情况（作为血管刺激的体外标志物），并测量SNP、异丙肾上腺素、多巴酚丁胺或尼莫地平的作用。
有血管痉挛证据的SAH患者的CSF将氧消耗刺激至0.91±0.17（微摩尔氧/分钟/克干重，±标准差，p≤0.01），而无血管痉挛的SAH患者的CSF未显著刺激氧消耗（0.27±0.02，猪颈动脉未刺激的呼吸速率为0.23±0.03微摩尔氧/分钟/克干重）。SNP、异丙肾上腺素或多巴酚丁胺显著（p≤0.01）降低了猪颈动脉氧消耗的刺激，而尼莫地平则没有。在41例单独接受尼莫地平或尼莫地平与多巴酚丁胺联合治疗的SAH患者队列中，仅接受尼莫地平治疗的患者住院死亡率为42%，而尼莫地平加多巴酚丁胺组的住院死亡率为17%（P≤0.076）。
41例患者的体内数据无统计学意义，因此需要进一步研究以确定这些差异是否重要。SNP、异丙肾上腺素和多巴酚丁胺显著降低了暴露于有血管痉挛的SAH患者CSF中的猪颈动脉的氧消耗，而尼莫地平则没有。我们的体外研究结果表明，这些化合物需要在有血管痉挛风险的SAH患者中进一步研究，因为它们可能对痉挛血管有直接益处。
