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Transvenous Diaphragm Neurostimulation Mitigates Ventilation-associated Brain Injury.
American Journal of Respiratory and Critical Care Medicine ( IF 19.3 ) Pub Date : 2021-12-15 , DOI: 10.1164/rccm.202101-0076oc
Thiago G Bassi 1, 2 , Elizabeth C Rohrs 1, 3 , Karl C Fernandez 1, 3 , Marlena Ornowska 1 , Michelle Nicholas 1, 3 , Matt Gani 2 , Doug Evans 2 , Steven C Reynolds 1, 3
Affiliation  

Rationale: Mechanical ventilation (MV) is associated with hippocampal apoptosis and inflammation, and it is important to study strategies to mitigate them. Objectives: To explore whether temporary transvenous diaphragm neurostimulation (TTDN) in association with MV mitigates hippocampal apoptosis and inflammation after 50 hours of MV. Methods: Normal-lung porcine study comparing apoptotic index, inflammatory markers, and neurological-damage serum markers between never-ventilated subjects, subjects undergoing 50 hours of MV plus either TTDN every other breath or every breath, and subjects undergoing 50 hours of MV (MV group). MV settings in volume control were Vt of 8 ml/kg, and positive end-expiratory pressure of 5 cm H2O. Measurements and Main Results: Apoptotic indices, microglia percentages, and reactive astrocyte percentages were greater in the MV group in comparison with the other groups (P < 0.05). Transpulmonary pressure at baseline and at study end were both lower in the group receiving TTDN every breath, but lung injury scores and systemic inflammatory markers were not different between the groups. Serum concentrations of four neurological-damage markers were lower in the group receiving TTDN every breath than in the MV group (P < 0.05). Heart rate variability declined significantly in the MV group and increased significantly in both TTDN groups over the course of the experiments. Conclusions: Our study found that mechanical ventilation is associated with hippocampal apoptosis and inflammation, independent of lung injury and systemic inflammation. Also, in a porcine model, TTDN results in neuroprotection after 50 hours, and the degree of neuroprotection increases with greater exposure to TTDN.

中文翻译:


经静脉隔膜神经刺激减轻通气相关的脑损伤。



理由:机械通气(MV)与海马细胞凋亡和炎症有关,研究减轻这些症状的策略非常重要。目的:探讨与 MV 相关的临时经静脉膈肌神经刺激 (TTDN) 是否可以减轻 MV 50 小时后海马细胞凋亡和炎症。方法:正常肺猪研究比较了从未通气受试者、接受 50 小时 MV 加每隔一次呼吸或每次呼吸 TTDN 的受试者以及接受 50 小时 MV 的受试者之间的细胞凋亡指数、炎症标志物和神经损伤血清标志物。 MV组)。容量控制中的 MV 设置为 Vt 为 8 ml/kg,呼气末正压为 5 cm H2O。测量和主要结果:与其他组相比,MV 组的细胞凋亡指数、小胶质细胞百分比和反应性星形胶质细胞百分比更高 (P < 0.05)。每次呼吸接受 TTDN 的组的基线和研究结束时的跨肺压均较低,但各组之间的肺损伤评分和全身炎症标志物没有差异。每次呼吸接受 TTDN 的组中四种神经损伤标志物的血清浓度低于 MV 组 (P < 0.05)。在实验过程中,MV 组的心率变异性显着下降,而 TTDN 组的心率变异性则显着增加。结论:我们的研究发现机械通气与海马细胞凋亡和炎症相关,与肺损伤和全身炎症无关。此外,在猪模型中,TTDN 在 50 小时后产生神经保护作用,并且神经保护程度随着 TTDN 暴露量的增加而增加。
更新日期:2021-09-07
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