Severe hemodilutional anemia increases cerebral tissue injury following acute neurotrauma
Severe hemodilutional anemia increases cerebral tissue injury following acute neurotrauma
复制标题
DOI：
10.1152/japplphysiol.01315.2006
复制
发表时间：
2007-09-01
影响因子：
3.3
通讯作者：
Baker, Andrew J.
中科院分区：
文献类型：
--
作者：
Hare, Gregory M. T.;Mazer, C. David;Baker, Andrew J.
贫血可能会恶化创伤性脑损伤（TBI）后的神经功能结局，其机制尚不明确。我们假设血液稀释性贫血加重了TBI后的缺氧性脑损伤。麻醉大鼠进行单侧TBI或假损伤（n >= 7）。通过用pentastarch交换40-50%的血容量（1：1）实现50 - 70 g/ l的目标血红蛋白浓度。通过测量脑组织氧分压（PbrO（2））、局部脑血流量（rCBF）、颈静脉血氧饱和度（SjvO（2））、脑挫伤面积和程序性细胞死亡的核染色来评估TBI、贫血和TBI-贫血的影响。TBI组和TBI贫血组的基线损伤后PbrO 2值（分别为9.3 +/- 1.3和11.3 +/- 4.1 Torr）低于未损伤对照组（18.2 +/- 5.2 Torr，P < 0.05）。相对于无贫血的TBI组，血液稀释导致TBI贫血组的PbO 2进一步降低（7.8 +/- 2.7 vs. 14.8 +/- 3.9 Torr，P < 0.05）。贫血组和TBI合并贫血组的rCBF在TBI后保持稳定，在血液稀释后增加。TBI后SjvO（2）升高（87.4 ± 8.9%，P < 0.05），血液稀释后进一步升高（95.0 ± 1.6%，P < 0.05）。脑挫伤面积和程序性细胞死亡的核计数在TBI贫血后（分别为4.1 +/- 3.0 mm 2和686 +/- 192）相对于单独TBI（分别为1.3 +/- 0.3 mm 2和404 +/- 133，P均< 0.05）增加。血液稀释性贫血减少脑PbO（2）和氧提取，并增加TBI后的细胞死亡。这些结果支持我们的假设，急性贫血加重缺氧性脑损伤后神经创伤。
Anemia may worsen neurological outcomes following traumatic brain injury (TBI) by undefined mechanisms. We hypothesized that hemodilutional anemia accentuates hypoxic cerebral injury following TBI. Anesthetized rats underwent unilateral TBI or sham injury (n >= 7). Target hemoglobin concentrations between 50 and 70 g/ l were achieved by exchanging 40-50% of the blood volume (1: 1) with pentastarch. The effect of TBI, anemia, and TBI-anemia was assessed by measuring brain tissue oxygen tension (PbrO(2)), regional cerebral blood flow (rCBF), jugular venous oxygen saturation (SjvO(2)), cerebral contusion area, and nuclear staining for programmed cell death. Baseline postinjury PbrO2 values in the TBI and TBI-anemia groups (9.3 +/- 1.3 and 11.3 +/- 4.1 Torr, respectively) were lower than the uninjured controls (18.2 +/- 5.2 Torr, P < 0.05 for both). Hemodilution caused a further reduction in PbrO2 in the TBI-anemia group relative to the TBI group without anemia (7.8 +/- 2.7 vs. 14.8 +/- 3.9 Torr, P < 0.05). The rCBF remained stable after TBI and increased comparably after hemodilution in both anemia and TBI-anemia groups. The SjvO(2) was elevated after TBI (87.4 +/- 8.9%, P < 0.05) and increased further following hemodilution (95.0 +/- 1.6%, P < 0.05). Cerebral contusion area and nuclear counts for programmed cell death were increased following TBI-anemia (4.1 +/- 3.0 mm2 and 686 +/- 192, respectively) relative to TBI alone (1.3 +/- 0.3 mm2 and 404 +/- 133, respectively, P < 0.05 for both). Hemodilutional anemia reduced cerebral PbrO(2) and oxygen extraction and increased cell death following TBI. These results support our hypothesis that acute anemia accentuated hypoxic cerebral injury after neurotrauma.