HYPERTENSION WITH HEMODILUTION PREVENTS MULTIFOCAL CEREBRAL HYPOPERFUSION AFTER CARDIAC-ARREST IN DOGS
HYPERTENSION WITH HEMODILUTION PREVENTS MULTIFOCAL CEREBRAL HYPOPERFUSION AFTER CARDIAC-ARREST IN DOGS
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DOI：
10.1161/01.str.23.1.45
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发表时间：
1992-01-01
期刊：
影响因子：
8.3
通讯作者：
OKU, K
中科院分区：
文献类型：
--
作者：
LEONOV, Y;STERZ, F;OKU, K
背景资料：在早期研究中，静息后高血压血液稀释改善神经功能结局可能是更均匀的脑灌注和改善O2输送的结果。我们探讨了全球，区域和当地的脑血流量稳定氙增强计算机断层扫描和全球脑代谢在我们的狗cardiac arrest model.Methods：心室颤动心脏骤停12.5分钟逆转简短的体外循环，随后生命支持4小时postarrest。我们比较了对照组I（n = 5;平均动脉血压，100 mm Hg;红细胞压积，大于或等于35%），静息后即刻再灌注促进组II（n = 5;平均动脉血压，140-110 mm Hg;用血浆替代品进行高容量血液稀释，红细胞压积为20-25%）。在两组的初始充血后，在休息后1-4小时的“延迟低灌注期”期间，I组的总体脑血流量为基线的51-60%，而II组为基线的85-100%（p < 6.01）。组II中无血流、滴流或低血流的脑组织体素的体积较低（p < 0.01），平均局部脑血流量值较高（p < 0.01）。两组的总体脑氧摄取在休息后3-4小时恢复到接近基线值。然而，血液稀释组II的静息后动脉O2含量为组I的40-50%。因此，O2摄取/输送比增加（恶化）在两组postarrest.Conclusions：长时间心脏停搏后，立即诱导中度高血压血液稀释到红细胞压积20-25%可以正常化脑血流模式（改善脑灌注的均匀性），但并没有改善脑O2输送，因为流量的好处是由动脉O2含量降低抵消。需要个体化滴定红细胞压积或使用无细胞O2携带血液替代品（无基质血红蛋白或氟碳溶液）进行血液稀释，以提高O2摄取/输送率。
Background: Improved neurological outcome with postarrest hypertensive hemodilution in an earlier study could be the result of more homogeneous cerebral perfusion and improved O2 delivery. We explored global, regional, and local cerebral blood flow by stable xenon-enhanced computed tomography and global cerebral metabolism in our dog cardiac arrest model.Methods: Ventricular fibrillation cardiac arrest of 12.5 minutes was reversed by brief cardiopulmonary bypass, followed by life support to 4 hours postarrest. We compared control group I (n = 5; mean arterial blood pressure, 100 mm Hg; hematocrit, greater-than-or-equal-to 35%) with immediately postarrest reflow-promoted group II (n = 5; mean arterial blood pressure, 140-110 mm Hg; hypervolemic hemodilution with plasma substitute to hematocrit, 20-25%).Results: After initial hyperemia in both groups, during the "delayed hypoperfusion phase" at 1-4 hours postarrest, global cerebral blood flow was 51-60% of baseline in group I versus 85-100% of baseline in group II (p < 6.01). Percentages of brain tissue voxels with no flow, trickle flow, or low flow were lower (p < 0.01) and mean regional cerebral blood flow values were higher in group II (p < 0.01). Global cerebral oxygen uptake recovered to near baseline values at 3-4 hours postarrest in both groups. Postarrest arterial O2 content, however, in hemodiluted group II was 40-50% of that in group I. Thus, the O2 uptake/delivery ratio was increased (worsened) in both groups at 2-4 hours postarrest.Conclusions: After prolonged cardiac arrest, immediately induced moderate hypertensive hemodilution to hematocrit 20-25% can normalize cerebral blood flow patterns (improve homogeneity of cerebral perfusion), but does not improve cerebral O2 delivery, since the flow benefit is offset by decreased arterial O2 content. Individualized titration of hematocrit or hemodilution with acellular O2 carrying blood substitute (stroma-free hemoglobin or fluorocarbon solution) would be required to improve O2 uptake/delivery ratio.