Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, Seongnamsi, Kyoneggido, Korea.
Anesth Analg. 2012 Jun;114(6):1285-91. doi: 10.1213/ANE.0b013e31824d2723. Epub 2012 Mar 26.
Acute normovolemic hemodilution (ANH) is currently performed during thoracoabdominal aortic surgery. However, the effects of ANH on spinal cord ischemic injury are currently unknown. Because hemodilution below a certain level of hematocrit (Hct) aggravates the neurological damage after cerebral ischemia, we hypothesized that ANH may increase neurological damage after spinal cord ischemia. The aim of these experiments was to determine the effects of ANH on spinal cord ischemic injury.
Thirty male Sprague-Dawley rats were randomly assigned to 1 of the following 3 groups: no hemodilution (group C), target Hct level of 30% (group HD30), and target Hct level of 25% (group HD25). ANH was performed upon withdrawal of blood and simultaneous replacement with the same volume with hydroxyethyl starch. Spinal cord ischemia and reperfusion were induced by using a balloon-tipped catheter placed in the descending thoracic aorta, and changes in mean arterial blood pressure were recorded. Neurological function of the hindlimbs was evaluated for 7 days and recorded using a motor deficit score (MDS) (0 = normal; 5 = complete paraplegia). The number of motor neurons within the spinal cord was counted after final MDS evaluation.
Group HD25 developed hypotension during the latter part of the ANH procedure. Group C and group HD30 experienced 3 minutes of reperfusion hypotension, whereas 6 minutes of hypotension was observed in group HD25. Two rats in group HD25 died during the experimental period. Seven days after reperfusion, the MDS of group C, group HD30, and group HD25 was 1.0 (0.5-2.0), 1.0 (0.5-2.0), and 4.0 (2.8-4.2) (median [95% confidence interval]), respectively. Group HD25 showed significantly higher MDS compared with group C (corrected P = 0.0018; 95% CI for median difference = 1.0-3.5). Motor neuron numbers in the anterior horns of group C, group HD30, and group HD25 were 26.5 (25.0-27.5), 23.5 (22.0-26.5), and 12.5 (8.4-16.6) (median [95% CI]), respectively. Motor neuron numbers of group HD25 were significantly lower than those of group C (corrected P < 0.0001; 95% CI for median difference = 9.0-18.0).
The results of the present study indicate that intraoperative ANH to an Hct of 25%, combined with coincident hypotension, caused a delayed recovery of baseline mean arterial blood pressure during the reperfusion period and aggravated neurological outcome after spinal cord ischemia.
急性等容血液稀释(ANH)目前在胸腹主动脉手术中进行。然而,ANH 对脊髓缺血性损伤的影响目前尚不清楚。由于血液稀释至一定的血细胞比容(Hct)水平以下会加重脑缺血后的神经损伤,我们假设 ANH 可能会增加脊髓缺血后的神经损伤。这些实验的目的是确定 ANH 对脊髓缺血性损伤的影响。
30 只雄性 Sprague-Dawley 大鼠随机分为以下 3 组:无血液稀释组(C 组)、目标 Hct 水平 30%组(HD30 组)和目标 Hct 水平 25%组(HD25 组)。通过从大鼠体内抽取血液并用相同体积的羟乙基淀粉替代,进行 ANH。使用放置在降主动脉的球囊尖端导管诱导脊髓缺血再灌注,并记录平均动脉血压的变化。在最后一次 MDS 评估后,通过运动缺陷评分(MDS)(0 = 正常;5 = 完全截瘫)评估后肢的神经功能,连续 7 天记录。
HD25 组在 ANH 过程的后半段出现低血压。C 组和 HD30 组经历了 3 分钟的再灌注低血压,而 HD25 组则经历了 6 分钟的低血压。HD25 组有 2 只大鼠在实验期间死亡。再灌注后 7 天,C 组、HD30 组和 HD25 组的 MDS 分别为 1.0(0.5-2.0)、1.0(0.5-2.0)和 4.0(2.8-4.2)(中位数[95%置信区间])。与 C 组相比,HD25 组的 MDS 明显更高(校正 P = 0.0018;中位数差值的 95%置信区间为 1.0-3.5)。C 组、HD30 组和 HD25 组前角的运动神经元数量分别为 26.5(25.0-27.5)、23.5(22.0-26.5)和 12.5(8.4-16.6)(中位数[95%置信区间])。HD25 组的运动神经元数量明显低于 C 组(校正 P < 0.0001;中位数差值的 95%置信区间为 9.0-18.0)。
本研究结果表明,术中 ANH 至 Hct 水平 25%,同时伴有低血压,导致脊髓缺血再灌注期间基础平均动脉血压恢复延迟,并加重脊髓缺血后的神经功能预后。