Department of Hyperbaric Oxygen Medicine, Affiliated Nantong Rehabilitation Hospital of Nantong University, Nantong, Jiangsu Province, China.
Department of Rehabilitation Medicine, Affiliated Nantong Rehabilitation Hospital of Nantong University, Nantong, Jiangsu Province, China.
Med Gas Res. 2025 Mar 1;15(1):171-179. doi: 10.4103/mgr.MEDGASRES-D-24-00044. Epub 2024 Sep 25.
Oxygen therapy after acute lung injury can regulate the inflammatory response and reduce lung tissue injury. However, the optimal exposure pressure, duration, and frequency of oxygen therapy for acute lung injury remain unclear. In the present study, after intraperitoneal injection of lipopolysaccharide in ICR mice, 1.0 atmosphere absolute (ATA) pure oxygen and 2.0 ATA hyperbaric oxygen treatment for 1 hour decreased the levels of proinflammatory factors (interleukin-1beta and interleukin-6) in peripheral blood and lung tissues. However, only 2.0 ATA hyperbaric oxygen increased the mRNA levels of anti-inflammatory factors (interleukin-10 and arginase-1) in lung tissue; 3.0 ATA hyperbaric oxygen treatment had no significant effect. We also observed that at 2.0 ATA, the anti-inflammatory effect of a single exposure to hyperbaric oxygen for 3 hours was greater than that of a single exposure to hyperbaric oxygen for 1 hour. The protective effect of two exposures for 1.5 hours was similar to that of a single exposure for 3 hours. These results suggest that hyperbaric oxygen alleviates lipopolysaccharide-induced acute lung injury by regulating the expression of inflammatory factors in an acute lung injury model and that appropriately increasing the duration and frequency of hyperbaric oxygen exposure has a better tissue-protective effect on lipopolysaccharide-induced acute lung injury. These results could guide the development of more effective oxygen therapy regimens for acute lung injury patients.
急性肺损伤后氧疗可以调节炎症反应,减轻肺组织损伤。然而,急性肺损伤患者接受氧疗的最佳暴露压力、时间和频率仍不清楚。在本研究中,在 ICR 小鼠腹腔注射脂多糖后,1.0 个大气压绝对(ATA)纯氧和 2.0ATA 高压氧治疗 1 小时,降低了外周血和肺组织中促炎因子(白细胞介素-1β和白细胞介素-6)的水平。然而,只有 2.0ATA 高压氧增加了肺组织中抗炎因子(白细胞介素-10 和精氨酸酶-1)的 mRNA 水平;3.0ATA 高压氧处理没有显著效果。我们还观察到,在 2.0ATA 时,单次高压氧暴露 3 小时的抗炎作用大于单次高压氧暴露 1 小时。两次 1.5 小时暴露的保护作用与单次 3 小时暴露的保护作用相似。这些结果表明,高压氧通过调节急性肺损伤模型中炎症因子的表达来缓解脂多糖诱导的急性肺损伤,适当增加高压氧暴露的时间和频率对脂多糖诱导的急性肺损伤具有更好的组织保护作用。这些结果可以为急性肺损伤患者的氧疗方案提供指导。