Bickenbach Johannes, Zoremba Norbert, Fries Michael, Dembinski Rolf, Doering Robert, Ogawa Eileen, Rossaint Rolf, Kuhlen Ralf
Department of Surgical Intensive Care, RWTH University Hospital, Aachen, Germany.
Anesth Analg. 2009 Sep;109(3):847-55. doi: 10.1213/ane.0b013e3181ad5769.
In study, we investigated the effects of different tidal volumes on cerebral tissue oxygenation and cerebral metabolism in a porcine model of acute lung injury (ALI). We hypothesized that mechanical ventilation with low tidal (LT) volumes improves cerebral tissue oxygenation and metabolism after experimentally induced ALI.
After inducing experimental ALI by surfactant depletion, we studied two conditions in 10 female pigs: 1) LT volume ventilation with 6 mL/kg body weight, and 2) high tidal (HT) volume ventilation with 12 mL/kg body weight. Variables of gas exchange, hemodynamic, continuous cerebral tissue oxygen tension (p(ti)O2), cerebral microdialysis, and systemic cytokines were analyzed. After induction of ALI, data were collected at 2, 4, and 8 h. The primary end point was the change in p(ti)O2. For group comparisons, a t-test was used. A value of <0.05 was considered to indicate statistical significance.
At baseline and after induction of ALI, no differences between groups were found in p(ti)O2; however, p(ti)O2 was significantly lower in the HT group after 4 and 8 h. PaO2 and PaCO2 showed no significant differences between the groups at all timepoints. Regarding cerebral microdialysis, a significantly higher level of extracellular lactate could be demonstrated after 2, 4, and 8 h in the HT group. The release of cytokines resulted in higher values for interleukin-6 and interleukin-8 in the HT group.
Protective ventilation with LT yielded a significant improvement in cerebral tissue oxygenation and metabolism compared to HT ventilation in a porcine model of ALI. There was dissociation between arterial and cerebral tissue oxygenation. Cerebral oxygenation and metabolism might have possibly been impaired by a more distinctive inflammatory response in the HT group.
在本研究中,我们在猪急性肺损伤(ALI)模型中研究了不同潮气量对脑组织氧合和脑代谢的影响。我们假设,在实验性诱导ALI后,低潮气量(LT)机械通气可改善脑组织氧合和代谢。
通过表面活性剂耗竭诱导实验性ALI后,我们在10只雌性猪中研究了两种情况:1)6 mL/kg体重的LT通气,以及2)12 mL/kg体重的高潮气量(HT)通气。分析了气体交换、血流动力学、连续脑组织氧张力(p(ti)O2)、脑微透析和全身细胞因子的变量。在诱导ALI后,于2、4和8小时收集数据。主要终点是p(ti)O2的变化。进行组间比较时使用t检验。P<0.05被认为具有统计学意义。
在基线和诱导ALI后,两组之间的p(ti)O2无差异;然而,4小时和8小时后HT组的p(ti)O2显著降低。所有时间点两组之间的PaO2和PaCO2均无显著差异。关于脑微透析,HT组在2、4和8小时后细胞外乳酸水平显著更高。细胞因子的释放导致HT组白细胞介素-6和白细胞介素-8的值更高。
在猪ALI模型中,与HT通气相比,LT保护性通气可显著改善脑组织氧合和代谢。动脉氧合与脑组织氧合之间存在分离。HT组更明显的炎症反应可能损害了脑氧合和代谢。