Cannizzaro Vincenzo, Berry Luke J, Nicholls Philip K, Hantos Zoltán, Sly Peter D
Division of Clinical Sciences, Telethon Institute for Child Health Research, Centre for Child Health Research, the University of Western Australia, Perth, Australia.
J Trauma. 2010 Oct;69(4):E24-31. doi: 10.1097/TA.0b013e3181d7503c.
Both high tidal volume (V(T)) ventilation and hemorrhage induce acute lung injury in adult rodents. It is not known whether injurious ventilation augments lung injury in infant rats exposed to severe hemorrhage.
Two-week-old rats were allocated for ventilation with VT 7 mL/kg and positive end-expiratory pressure (PEEP) 5 cm H₂O (low V(T)) or V(T) 21 mL/kg and PEEP 1 (high V(T)) for 4 hours. Additional rats were subjected to volume-controlled hemorrhage and delayed saline resuscitation, followed by low V(T) or high V(T) ventilation for 4 hours. Nonventilated control groups were also included. Airway resistance and the coefficient of tissue elastance were derived from respiratory input impedance measurements using the low-frequency forced oscillation technique. Pressure-volume curves were obtained at baseline and at the end of the study. Interleukin-6, macrophage inflammatory protein-2, and tumor necrosis factor alpha were determined in bronchoalveolar lavage fluid (BALF) and serum.
In both healthy and hemorrhage-exposed animals, high V(T) resulted in reduced elastance (better lung compliance) and increased transcutaneous oxygen saturation. Interleukin-6 in BALF was greater in ventilated animals when compared with nonventilated controls, but not different among ventilated groups. No significant differences were found for all other inflammatory mediators, total protein concentration in BALF, and histology.
High V(T) ventilation with low PEEP improves respiratory system mechanics without causing additional damage to healthy and hemorrhage-exposed infant rats after 4 hours of ventilation. This study highlights the tolerance to high V(T) ventilation in infant rats and underscores the need for age-specific animal models.
高潮气量(V(T))通气和出血均可诱导成年啮齿动物发生急性肺损伤。目前尚不清楚有害通气是否会加重暴露于严重出血的幼鼠的肺损伤。
将两周龄的大鼠分为两组,一组以7 mL/kg的潮气量(VT)和5 cm H₂O的呼气末正压(PEEP)(低潮气量)通气,另一组以21 mL/kg的VT和1 cm H₂O的PEEP(高潮气量)通气4小时。另外的大鼠进行容量控制性出血并延迟生理盐水复苏,然后分别进行低潮气量或高潮气量通气4小时。同时设置非通气对照组。使用低频强迫振荡技术通过呼吸输入阻抗测量得出气道阻力和组织弹性系数。在基线和研究结束时获取压力-容积曲线。测定支气管肺泡灌洗液(BALF)和血清中的白细胞介素-6、巨噬细胞炎性蛋白-2和肿瘤坏死因子α。
在健康和出血暴露的动物中,高潮气量均导致弹性降低(肺顺应性更好)和经皮氧饱和度增加。与非通气对照组相比,通气动物的BALF中的白细胞介素-6含量更高,但通气组之间无差异。在所有其他炎症介质、BALF中的总蛋白浓度和组织学方面均未发现显著差异。
低潮气量的高潮气量通气可改善呼吸系统力学,在通气4小时后不会对健康和出血暴露的幼鼠造成额外损伤。本研究强调了幼鼠对高潮气量通气的耐受性,并强调了建立特定年龄动物模型的必要性。