Protective ventilation with lower tidal volumes reduces systemic and organ-specific inflammation. In sepsis-induced encephalopathy or acute brain injury the use of protective ventilation has not been widely investigated (experimentally or clinically). We hypothesized that protective ventilation would attenuate cerebral inflammation in a porcine endotoxemic sepsis model. The aim of the study was to study the effect of tidal volume on cerebral inflammatory response, cerebral metabolism and brain injury. Nine animals received protective mechanical ventilation with a tidal volume of 6 mL × kg−1 and nine animals were ventilated with a tidal volume of 10 mL × kg−1. During a 6-h experiment, the pigs received an endotoxin intravenous infusion of 0.25 µg × kg−1 × h−1. Systemic, superior sagittal sinus and jugular vein blood samples were analysed for inflammatory cytokines and S100B. Intracranial pressure, brain tissue oxygenation and brain microdialysis were sampled every hour. No differences in systemic or sagittal sinus levels of TNF-α or IL-6 were seen between the groups. The low tidal volume group had increased cerebral blood flow (p < 0.001) and cerebral oxygen delivery (p < 0.001), lower cerebral vascular resistance (p < 0.05), higher cerebral metabolic rate (p < 0.05) along with higher cerebral glucose consumption (p < 0.05) and lactate production (p < 0.05). Moreover, low tidal volume ventilation increased the levels of glutamate (p < 0.01), glycerol (p < 0.05) and showed a trend towards higher lactate to pyruvate ratio (p = 0.08) in cerebral microdialysate as well as higher levels of S-100B (p < 0.05) in jugular venous plasma compared with medium–high tidal volume ventilation. Contrary to the hypothesis, protective ventilation did not affect inflammatory cytokines. The low tidal volume group had increased cerebral blood flow, cerebral oxygen delivery and cerebral metabolism together with increased levels of markers of brain injury compared with medium–high tidal volume ventilation.

中文翻译：

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肺保护性通气增加猪实验性脓毒症的脑代谢和非炎症性脑损伤

具有较低潮气量的保护性通气可减少全身性和器官特异性炎症。在脓毒症引起的脑病或急性脑损伤中，保护性通气的使用尚未得到广泛研究（实验或临床）。我们假设保护性通气会减轻猪内毒素脓毒症模型中的脑部炎症。本研究的目的是研究潮气量对脑炎症反应、脑代谢和脑损伤的影响。九只动物接受了潮气量为 6 mL × kg-1 的保护性机械通气，九只动物接受了潮气量为 10 mL × kg-1 的通气。在 6 小时的实验中，猪接受了 0.25 µg × kg-1 × h-1 的内毒素静脉输注。系统性的，分析上矢状窦和颈静脉血样的炎性细胞因子和 S100B。每小时对颅内压、脑组织氧合和脑微透析进行采样。两组之间未观察到 TNF-α 或 IL-6 的全身或矢状窦水平有差异。低潮气量组脑血流量增加（p < 0.001）和脑氧输送增加（p < 0.001），脑血管阻力降低（p < 0.05），脑代谢率提高（p < 0.05），同时脑葡萄糖消耗增加(p < 0.05) 和乳酸产量 (p < 0.05)。此外，低潮气量通气增加了谷氨酸 (p < 0.01)、甘油 (p < 0.05) 的水平，并显示出乳酸与丙酮酸比率升高的趋势 (p = 0. 08) 在脑微透析液中以及与中高潮气量通气相比，颈静脉血浆中更高水平的 S-100B (p < 0.05)。与假设相反，保护性通气不影响炎性细胞因子。与中高潮气量通气相比，低潮气量组脑血流量、脑氧输送和脑代谢增加，脑损伤标志物水平升高。