Ekelund A, Reinstrup P, Ryding E, Andersson A-M, Molund T, Kristiansson K-A, Romner B, Brandt L, Säveland H
Department of Neurosurgery, University Hospital, Lund, Sweden.
Acta Neurochir (Wien). 2002 Jul;144(7):703-12; discussion 712-3. doi: 10.1007/s00701-002-0959-9.
Arterial vasospasm after subarachnoid hemorrhage may cause cerebral ischemia. Treatment with hemodilution, reducing blood viscosity, and hypervolemia, increasing cardiac performance and distending the vasospastic artery, are clinically established methods to improve blood flow through the vasospastic arterial bed.
Eight patients with transcranial Doppler verified vasospasm after subarachnoid hemorrhage were investigated with global (two-dimensional (133)Xenon) and regional (three-dimensional (99 m)Tc-HMPAO) cerebral blood flow (CBF) measurements, before and after 1/iso- and 2/hypervolemic hemodilution. Hematocrit was reduced to 0.28 from 0.36. Hypervolemia was achieved by increasing blood volume by 1100 ml.
Isovolemic hemodilution increased global cerebral blood flow from 52.25+/-10.12 to 58.56+/-11.73 ml * 100 g(-1) * min(-1) (p<0.05), but after hypervolemic hemodilution CBF returned to 51.38+/-11.34 ml * 100 g(-1) * min(-1). Global cerebral delivery rate of oxygen (CDRO(2)) decreased from 7.94+/-1.92 to 6.98+/-1.66 ml * 100 g(-1) * min(-1) (p<0.001) during isovolemic hemodilution and remained reduced, 6.77+/-1.60 ml * 100 g(-1) * min(-1) (p<0.001), after the hypervolemic hemodilution. As a test of the hemodilution effect on regional CDRO(2) an ischemic threshold was defined as the maximal amount of oxygen transported by a CBF of 10 ml * 100 g(-1) * min(-1) at a Hb 140 g/l which corresponds to a CDRO(2) of 1.83 ml * 100 g(-1) * min(-1). The brain volume with a CDRO(2) exceeding the ichemic threshold was 1300+/-236 ml before intervention. After isovolemic hemodilution the non-ischemic brain volume was reduced to 1206+/-341 (p<0,003). After hypervolemic hemodilution the non-ischemic brain volume remained reduced at 1228+/-347 ml (p<0.05).
The present study of controlled isovolemic hemodilution demonstrated increased global CBF, but there was a pronounced reduction in oxygen delivery capacity. Both CBF and CDRO(2) remained decreased during further hypervolemic hemodilution. We conclude that hemodilution to hematocrit 0.28 is not beneficial for patients with cerebral vasospasm after SAH.
蛛网膜下腔出血后动脉血管痉挛可能导致脑缺血。血液稀释（降低血液粘度）和高血容量（增强心脏功能并扩张痉挛动脉）治疗是临床上已确立的改善通过痉挛动脉床血流的方法。
对8例经经颅多普勒证实蛛网膜下腔出血后血管痉挛的患者，在等容和高容血液稀释前后，采用整体（二维（133）氙）和局部（三维（99m）锝 - 六甲基丙二胺肟）脑血流量（CBF）测量。血细胞比容从0.36降至0.28。通过将血容量增加1100 ml实现高血容量。
等容血液稀释使整体脑血流量从52.25±10.12增加至58.56±11.73 ml·100 g⁻¹·min⁻¹（p<0.05），但高容血液稀释后CBF恢复至51.38±11.34 ml·100 g⁻¹·min⁻¹。等容血液稀释期间，整体脑氧输送率（CDRO₂）从7.94±1.92降至6.98±1.66 ml·100 g⁻¹·min⁻¹（p<0.001），高容血液稀释后仍降低，为6.77±1.60 ml·100 g⁻¹·min⁻¹（p<0.001）。作为血液稀释对局部CDRO₂影响的测试，缺血阈值定义为血红蛋白140 g/l时CBF为10 ml·100 g⁻¹·min⁻¹所输送的最大氧量，对应CDRO₂为1.83 ml·100 g⁻¹·min⁻¹。干预前CDRO₂超过缺血阈值的脑体积为1300±236 ml。等容血液稀释后，非缺血脑体积降至1206±341（p<0.003）。高容血液稀释后，非缺血脑体积仍降至1228±347 ml（p<0.05）。
本项关于控制性等容血液稀释的研究表明整体CBF增加，但氧输送能力显著降低。在进一步的高容血液稀释过程中，CBF和CDRO₂均持续降低。我们得出结论，将血细胞比容稀释至0.28对蛛网膜下腔出血后脑血管痉挛患者并无益处。
