Resuscitation Fluid with Drag Reducing Polymer Enhances Cerebral Microcirculation and Tissue Oxygenation After Traumatic Brain Injury Complicated by Hemorrhagic Shock.

Resuscitation Fluid with Drag Reducing Polymer Enhances Cerebral Microcirculation and Tissue Oxygenation After Traumatic Brain Injury Complicated by Hemorrhagic Shock.
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DOI:
10.1007/978-3-319-91287-5_7
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发表时间:
2018
影响因子:
--
通讯作者:
Nemoto EM
Nemoto EM
中科院分区:
医学4区
文献类型:
--
作者:
Bragin DE;Lara DA;Bragina OA;Kameneva MV;Nemoto EM

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创伤性脑损伤(Traumatic brain injury,TBI)常伴有出血性休克(hemorrhagic shock,HS),其发病率和死亡率显著增加。现有的用于容量扩张的复苏液(RF)不足以减轻TBI/HS后受损的微血管脑血流量(mvCBF)和缺氧。我们假设,在复苏液(DRP-RF)中的减阻聚合物的纳摩尔量,将通过血液动力学的流变学调节改善mvCBF。通过液压冲击(1.5 atm,50 ms)诱导大鼠TBI,然后控制出血至平均动脉压(MAP)= 40 mmHg。输注DRP-RF或乳酸林格氏液(LR-RF)至MAP为60 mmHg,持续1小时(入院前),然后再输注血液至MAP = 70 mmHg(入院)。监测体温、MAP、血气和电解质。在体内2-光子激光扫描显微镜用于监测微血管血流,缺氧(NADH)和坏死(静脉碘化丙啶)后5小时TBI/HS,然后通过MRI的CBF和病变体积。TBI/HS损害脑微血管流动,导致毛细血管微血栓形成、组织缺氧和神经元坏死。与LR-RF相比,DRP-RF减少了微血栓形成,恢复了塌陷的毛细血管血流并改善了mvCBF(分别为82 ± 9.7% vs. 62 ± 9.7%,p< 0.05,n = 10)。DRP-RF与LR-RF相比减少了组织缺氧(77 ± 8.2%对60 ± 10.5%,p< 0.05)和神经元坏死(分别为21 ± 7.2%对36 ± 7.3%,p< 0.05)。MRI显示DRP-RF的病变体积减小。与TBI/HS后使用LR-RF的常规容量扩张相比,DRP-RF有效地恢复mvCBF,减少缺氧并保护神经元。
Traumatic brain injury (TBI) is frequently accompanied by hemorrhagic shock (HS) which significantly worsens morbidity and mortality. Existing resuscitation fluids (RF) for volume expansion inadequately mitigate impaired microvascular cerebral blood flow (mvCBF) and hypoxia after TBI/HS. We hypothesized that nanomolar quantities of drag reducing polymers in resuscitation fluid (DRP-RF), would improve mvCBF by rheological modulation of hemodynamics. TBI was induced in rats by fluid percussion (1.5 atm, 50 ms) followed by controlled hemorrhage to a mean arterial pressure (MAP) = 40 mmHg. DRP-RF or lactated Ringer (LR-RF) was infused to MAP of 60 mmHg for 1 h (pre-hospital), followed by blood re-infusion to a MAP = 70 mmHg (hospital). Temperature, MAP, blood gases and electrolytes were monitored. In vivo 2-photon laser scanning microscopy was used to monitor microvascular blood flow, hypoxia (NADH) and necrosis (i.v. propidium iodide) for 5 h after TBI/HS followed by MRI for CBF and lesion volume. TBI/HS compromised brain microvascular flow leading to capillary microthrombosis, tissue hypoxia and neuronal necrosis. DRP-RF compared to LR-RF reduced microthrombosis, restored collapsed capillary flow and improved mvCBF (82 ± 9.7% vs. 62 ± 9.7%, respectively, p< 0.05, n = 10). DRP-RF vs LR-RF decreased tissue hypoxia (77 ± 8.2% vs. 60 ± 10.5%, p< 0.05), and neuronal necrosis (21 ± 7.2% vs. 36 ± 7.3%, respectively, p< 0.05). MRI showed reduced lesion volumes with DRP-RF. DRP-RF effectively restores mvCBF, reduces hypoxia and protects neurons compared to conventional volume expansion with LR-RF after TBI/HS.
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