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在失血性休克和严重颅脑损伤的实验模型中,低血压的治疗策略是否可以改善脑灌注和氧合?

Can a Therapeutic Strategy for Hypotension Improve Cerebral Perfusion and Oxygenation in an Experimental Model of Hemorrhagic Shock and Severe Traumatic Brain Injury?

机构信息

Anesthesiology Department, Hospital das Clinicas SP, School of Medicine, University of São Paulo, Av. Dr. Enéas de Carvalho Aguiar, 255, Cerqueira César, São Paulo, SP, 05403-000, Brazil.

Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.

出版信息

Neurocrit Care. 2023 Oct;39(2):320-330. doi: 10.1007/s12028-023-01802-5. Epub 2023 Aug 3.

Abstract

BACKGROUND

Restoration of brain tissue perfusion is a determining factor in the neurological evolution of patients with traumatic brain injury (TBI) and hemorrhagic shock (HS). In a porcine model of HS without neurological damage, it was observed that the use of fluids or vasoactive drugs was effective in restoring brain perfusion; however, only terlipressin promoted restoration of cerebral oxygenation and lower expression of edema and apoptosis markers. It is unclear whether the use of vasopressor drugs is effective and beneficial during situations of TBI. The objective of this study is to compare the effects of resuscitation with saline solution and terlipressin on cerebral perfusion and oxygenation in a model of TBI and HS.

METHODS

Thirty-two pigs weighing 20-30 kg were randomly allocated into four groups: control (no treatment), saline (60 ml/kg of 0.9% NaCl), terlipressin (2 mg of terlipressin), and saline plus terlipressin (20 ml/kg of 0.9% NaCl + 2 mg of terlipressin). Brain injury was induced by lateral fluid percussion, and HS was induced through pressure-controlled bleeding, aiming at a mean arterial pressure (MAP) of 40 mmHg. After 30 min of circulatory shock, resuscitation strategies were initiated according to the group. The systemic and cerebral hemodynamic and oxygenation parameters, lactate levels, and hemoglobin levels were evaluated. The data were subjected to analysis of variance for repeated measures. The significance level established for statistical analysis was p < 0.05.

RESULTS

The terlipressin and saline plus terlipressin groups showed an increase in MAP that lasted until the end of the experiment (p < 0.05). There was a notable increase in intracranial pressure in all groups after starting treatment for shock. Cerebral perfusion pressure and cerebral oximetry showed no improvement after hemodynamic recovery in any group. The groups that received saline at resuscitation had the lowest hemoglobin concentrations after treatment.

CONCLUSIONS

The treatment of hypotension in HS with saline and/or terlipressin cannot restore cerebral perfusion or oxygenation in experimental models of HS and severe TBI. Elevated MAP raises intracranial pressure owing to brain autoregulation dysfunction caused by TBI.

摘要

背景

恢复脑组织灌注是创伤性脑损伤(TBI)和出血性休克(HS)患者神经学演变的决定因素。在没有神经损伤的 HS 猪模型中,观察到使用液体或血管活性药物可有效恢复脑灌注;然而,只有特利加压素可促进脑氧合恢复和降低水肿和细胞凋亡标志物的表达。尚不清楚在 TBI 情况下使用升压药物是否有效和有益。本研究的目的是比较盐水和特利加压素复苏对 TBI 和 HS 模型中脑灌注和氧合的影响。

方法

32 头 20-30kg 的猪随机分为四组:对照组(无治疗)、生理盐水(60ml/kg 的 0.9% NaCl)、特利加压素(2mg 特利加压素)和生理盐水加特利加压素(20ml/kg 的 0.9% NaCl+2mg 特利加压素)。通过侧方液压冲击诱导脑损伤,通过压力控制出血诱导 HS,目标平均动脉压(MAP)为 40mmHg。循环休克 30min 后,根据组开始复苏策略。评估全身和脑血流动力学和氧合参数、乳酸水平和血红蛋白水平。数据采用重复测量方差分析。统计学分析的显著性水平设定为 p<0.05。

结果

特利加压素和生理盐水加特利加压素组的 MAP 升高持续到实验结束(p<0.05)。所有组在开始休克治疗后颅内压显著升高。在任何一组的血流动力学恢复后,脑灌注压和脑氧饱和度均无改善。在复苏时接受盐水的组在治疗后血红蛋白浓度最低。

结论

在 HS 和严重 TBI 的实验模型中,用盐水和/或特利加压素治疗低血压不能恢复脑灌注或氧合。MAP 的升高是由于 TBI 引起的脑自动调节功能障碍导致颅内压升高。

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