添加减阻聚合物到胶体复苏液可改善创伤性脑损伤合并失血性休克后脑微循环和组织氧合。

Addition of Drag-Reducing Polymers to Colloid Resuscitation Fluid Enhances Cerebral Microcirculation and Tissue Oxygenation After Traumatic Brain Injury Complicated by Hemorrhagic Shock.

机构信息

Lovelace Biomedical Research Institute, Albuquerque, NM, USA.

University of New Mexico School of Medicine, Departments of Neurology and Neurosurgery, Albuquerque, NM, USA.

出版信息

Adv Exp Med Biol. 2021;1269:283-288. doi: 10.1007/978-3-030-48238-1_45.

DOI:10.1007/978-3-030-48238-1_45

PMID:33966231

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9126076/

Abstract

Hemorrhagic shock (HS) is a severe complication of traumatic brain injury (TBI) that doubles mortality due to severely compromised microvascular cerebral blood flow (mvCBF) and oxygen delivery reduction, as a result of hypotension. Volume expansion with resuscitation fluids (RF) for HS does not improve microvascular CBF (mvCBF); moreover, it aggravates brain edema. We showed that the addition of drag-reducing polymers (DRP) to crystalloid RF (lactated Ringer's) significantly improves mvCBF, oxygen supply, and neuronal survival in rats suffering TBI+HS. Here, we compared the effects of colloid RF (Hetastarch) with DRP (HES-DRP) and without (HES). Fluid percussion TBI (1.5 ATA, 50 ms) was induced in rats and followed by controlled HS to a mean arterial pressure (MAP) of 40 mmHg. HES or HES-DRP was infused to restore MAP to 60 mmHg for 1 h (prehospital period), followed by blood reinfusion to a MAP of 70 mmHg (hospital period). In vivo two-photon microscopy was used to monitor cerebral microvascular blood flow, tissue hypoxia (NADH), and neuronal necrosis (i.v. propidium iodide) for 5 h after TBI+HS, followed by postmortem DiI vascular painting. Temperature, MAP, blood gases, and electrolytes were monitored. Statistical analyses were done using GraphPad Prism by Student's t-test or Kolmogorov-Smirnov test, where appropriate. TBI+HS compromised mvCBF and tissue oxygen supply due to capillary microthrombosis. HES-DRP improved mvCBF and tissue oxygenation (p < 0.05) better than HES. The number of dead neurons in the HES-DRP was significantly less than in the HES group: 76.1 ± 8.9 vs. 178.5 ± 10.3 per 0.075 mm (P < 0.05). Postmortem visualization of painted vessels revealed vast microthrombosis in both hemispheres that were 33 ± 2% less in HES-DRP vs. HES (p < 0.05). Thus, resuscitation after TBI+HS using HES-DRP effectively restores mvCBF and reduces hypoxia, microthrombosis, and neuronal necrosis compared to HES. HES-DRP is more neuroprotective than lactated Ringer's with DRP and requires an infusion of a smaller volume, which reduces the development of hypervolemia-induced brain edema.

摘要

失血性休克（HS）是创伤性脑损伤（TBI）的一种严重并发症，由于低血压导致脑微血管血流（mvCBF）严重受损和氧输送减少，死亡率增加一倍。HS 用复苏液（RF）进行容量扩张不能改善微血管 CBF（mvCBF）；此外，它会加重脑水肿。我们发现，向晶状 RF（乳酸林格氏液）中添加减阻聚合物（DRP）可显著改善 TBI+HS 大鼠的 mvCBF、氧供应和神经元存活。在这里，我们比较了胶体 RF（羟乙基淀粉）与 DRP（HES-DRP）和无 DRP（HES）的效果。在大鼠中诱导流体冲击性 TBI（1.5 ATA，50 ms），然后控制 HS 至平均动脉压（MAP）为 40 mmHg。HES 或 HES-DRP 输注以将 MAP 恢复至 60 mmHg 1 小时（院前期），然后再输血至 MAP 为 70 mmHg（医院期）。在 TBI+HS 后 5 小时内使用活体双光子显微镜监测脑微血管血流、组织缺氧（NADH）和神经元坏死（静脉注射碘化丙啶），然后进行死后 DiI 血管染色。监测体温、MAP、血气和电解质。使用 GraphPad Prism 通过 Student's t 检验或 Kolmogorov-Smirnov 检验进行统计分析，视情况而定。TBI+HS 由于毛细血管微血栓形成而导致 mvCBF 和组织氧供应受损。HES-DRP 改善 mvCBF 和组织氧合作用（p <0.05）优于 HES。HES-DRP 组的死亡神经元数量明显少于 HES 组：每 0.075 mm 为 76.1 ± 8.9 个 vs. 178.5 ± 10.3 个（p <0.05）。死后血管染色显示，两个半球均有广泛的微血栓形成，HES-DRP 组比 HES 组少 33 ± 2%（p <0.05）。因此，与 HES 相比，TBI+HS 后使用 HES-DRP 复苏可有效恢复 mvCBF，并减少缺氧、微血栓形成和神经元坏死。与含有 DRP 的乳酸林格氏液相比，HES-DRP 具有更好的神经保护作用，且所需输注体积更小，从而减少了高容量诱导性脑水肿的发生。