Reasoner D K, Ryu K H, Hindman B J, Cutkomp J, Smith T
Department of Anesthesia, College of Medicine, University of Iowa, Iowa City 52242, USA.
Anesth Analg. 1996 Jan;82(1):61-7. doi: 10.1097/00000539-199601000-00011.
Moderate hemodilution (hematocrit approximately 30%) reduces neurologic injury after focal cerebral ischemia. In contrast, both clinical and experimental studies suggest that marked hemodilution (hematocrit < 30%) may exacerbate neurologic injury. We compared the effect of marked versus minimal hemodilution on cerebral infarct volume after focal cerebral ischemia in rabbits. Anesthetized New Zealand White rabbits underwent hemodilution by exchange of arterial blood with 6% high molecular weight hydroxyethyl starch. In the marked hemodilution group (n = 15) the target hemoglobin concentration was 6 g/100 mL. In the minimal hemodilution group (n = 15) the target hemoglobin concentration was 11 g/100 mL. After hemodilution, middle cerebral artery occlusion was achieved by embolizing an autologous blood clot via the internal carotid artery. Four hours after embolization, the animals were killed and their brains removed. Brains were sectioned, stained with 2,3,5-triphenyltetrazolium chloride, and infarct volumes determined via quantitative image analysis. Systemic physiologic variables were similar between groups, except for arterial hemoglobin concentration. The percentage of hemispheric infarct was significantly larger in the marked hemodilution group as compared to the minimal hemodilution group, 70% +/- 19% vs 51% +/- 23%, respectively (mean +/- SD); P = 0.02. Similarly, the percentage of infarct was greater in the hemodilution group as compared to the minimal hemodilution group in both cortex (73% +/- 18% vs 54% +/- 23%, respectively; P = 0.02) and subcortex (62% +/- 25% vs 44% +/- 23%, respectively; P = 0.04). These findings indicate that marked hemodilution exacerbates neurologic injury resulting from permanent focal ischemia. Although some degree of hemodilution may improve neurologic outcome, the advantage is lost at an extreme level of therapy.
适度血液稀释（血细胞比容约为30%）可减轻局灶性脑缺血后的神经损伤。相比之下，临床和实验研究均表明，显著血液稀释（血细胞比容<30%）可能会加重神经损伤。我们比较了显著血液稀释与最小程度血液稀释对兔局灶性脑缺血后脑梗死体积的影响。对麻醉后的新西兰白兔通过用6%高分子量羟乙基淀粉交换动脉血进行血液稀释。在显著血液稀释组（n = 15）中，目标血红蛋白浓度为6 g/100 mL。在最小程度血液稀释组（n = 15）中，目标血红蛋白浓度为11 g/100 mL。血液稀释后，通过经颈内动脉栓塞自体血凝块实现大脑中动脉闭塞。栓塞后4小时，处死动物并取出大脑。将大脑切片，用2,3,5-三苯基氯化四氮唑染色，并通过定量图像分析确定梗死体积。除动脉血红蛋白浓度外，两组间全身生理变量相似。显著血液稀释组的半球梗死百分比明显高于最小程度血液稀释组，分别为70%±19%和51%±23%（均值±标准差）；P = 0.02。同样，在皮质（分别为73%±18%和54%±23%；P = 0.02）和皮质下（分别为62%±25%和44%±23%；P = 0.04），血液稀释组的梗死百分比均高于最小程度血液稀释组。这些发现表明，显著血液稀释会加重永久性局灶性缺血导致的神经损伤。虽然一定程度的血液稀释可能会改善神经预后，但在极端治疗水平下这种优势会丧失。
