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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Influence of tidal volume on pulmonary NO release, tissue lipid peroxidation and surfactant phospholipids
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Influence of tidal volume on pulmonary NO release, tissue lipid peroxidation and surfactant phospholipids

机译：潮气量对肺NO释放，组织脂质过氧化和表面活性剂磷脂的影响

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摘要

Mechanical stress during ventilation may cause or aggravate acute lung injury. This study investigates the influence of low vs. high tidal volume (V_t) on factors known to play key roles in acute lung injury: nitric oxide release, eNOS and iNOS gene expression, lipid peroxidation (LPO), and surfactant phospholipids (PL). Isolated rabbit lungs were subjected to one of three ventilation patterns for 135 min (V_t-PEEP): 6 ml/kg-0 cm H_2O, 12 ml/kg-0 cm H_2O, 6 ml/kg-5 cm H_2O. 12 ml/kg-0 cm H_2O and 6 ml/kg-5 cm H_2O resulted in comparable peak inspiratory pressure (PIP). This allowed comparing low and high V_t without dependence on PIP. Ventilatory patterns did not induce changes in pulmonary artery pressure, vascular permeability (K_(f,c)), PIP or pulmonary compliance. High V_t in comparison with both of the low V_t groups caused an increase in BALF-nitrite (30.6 ± 3.0~* vs. 21.4 ± 2.2 and 16.2 ± 3.3 μM), BALF-PL (1110 ± 19~* vs. 750 ± 68 and 634 ± 82 μg/ml), and tissue LPO product accumulation (0.62 ± 0.051~* vs. 0.48 ± 0.052 and 0.43 ± 0.031 mol/mg), ~*P < 0.05 each. Perfusate nitrite and BALF-PL composition (assessed by use of ~(31)P-NMR spectroscopy and MALDI-TOF mass spectrometry) did not differ among the groups. High V_t ventilation reduced eNOS gene expression but did not affect iNOS expression. The increased release of NO and the accumulation of LPO products may represent early lung injury while elevated BALF-PL may reflect distension-induced surfactant secretion.
机译：通风过程中的机械应力可能导致或加重急性肺损伤。这项研究调查了低潮气量和高潮气量（V_t）对已知在急性肺损伤中起关键作用的因素的影响：一氧化氮释放，eNOS和iNOS基因表达，脂质过氧化（LPO）和表面活性剂磷脂（PL）。对分离的兔肺进行三种通气模式之一，持续135分钟（V_t-PEEP）：6 ml / kg-0 cm H_2O，12 ml / kg-0 cm H_2O，6 ml / kg-5 cm H_2O。 12 ml / kg-0 cm H_2O和6 ml / kg-5 cm H_2O产生了相当的峰值吸气压力（PIP）。这允许在不依赖于PIP的情况下比较低V_t和高V_t。通气模式不会引起肺动脉压力，血管通透性（K_（f，c）），PIP或肺顺应性的变化。与低V_t组相比，高V_t导致BALF亚硝酸盐（30.6±3.0〜*与21.4±2.2和16.2±3.3μM），BALF-PL（1110±19〜*与750±68）的增加和634±82μg/ ml）和组织LPO产物积聚（0.62±0.051〜*与0.48±0.052和0.43±0.031 mol / mg），〜* P <0.05。组间亚硝酸灌流液和BALF-PL组成（通过〜（31）P-NMR光谱和MALDI-TOF质谱评估）没有差异。高Vt通气降低eNOS基因表达，但不影响iNOS表达。 NO的释放增加和LPO产物的积累可能代表早期肺损伤，而BALF-PL升高可能反映了扩张引起的表面活性剂分泌。

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