High tidal volume mechanical ventilation-induced lung injury in rats is greater after acid instillation than after sepsis-induced acute lung injury, but does not increase systemic inflammation: an experimental study.

High tidal volume mechanical ventilation-induced lung injury in rats is greater after acid instillation than after sepsis-induced acute lung injury, but does not increase systemic inflammation: an experimental study.
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DOI:
10.1186/1471-2253-11-26
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发表时间:
2011-12-28
期刊:
影响因子:
2.2
通讯作者:
Slutsky AS
Slutsky AS
中科院分区:
医学3区
文献类型:
--
作者:
Kuiper JW;Plötz FB;Groeneveld AJ;Haitsma JJ;Jothy S;Vaschetto R;Zhang H;Slutsky AS

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研究直接和间接来源的急性肺损伤对呼吸机诱导的肺损伤(VILI)和由此产生的全身炎症反应的易感性是否存在差异。采用酸滴注法或盲肠结扎穿刺法造成大鼠脓毒症2 4h后,给予低潮气量(Vt)为6 m L/kg、呼气末正压为5 cm H2O的机械通气(MV)或高Vt(15 m L/kg)、无PEEP(HVT酸、HVT脓毒症)。酸滴入后即刻处死大鼠,未通气的脓毒症动物作为对照。监测血流动力学和呼吸变量。4h后测定肺湿重/干重比、肺组织学损伤和血浆介质浓度。与脓毒症相比,酸滴入后氧合和肺顺应性降低。此外,与脓毒症相比,酸滴入后W/D重量比和组织学肺损伤评分增加。MV使肺湿重/干重比值和肺损伤评分增加,但这种作用主要归因于酸滴入后的HVT换气。同样,高压氧对氧合的影响只有在酸注入后才能观察到。脓毒症期间的HVT不会进一步影响氧合、顺应性、湿重/干重比或肺损伤评分。与脓毒症相比,酸液滴注后血浆IL-6和肿瘤坏死因子-α浓度升高,而细胞间黏附分子-1浓度仅在脓毒症时升高。与肺损伤指标相比,酸滴入后的HVT MV对血浆介质浓度没有额外的影响。在MV期间,与脓毒症相比,酸灌入后出现更严重的肺损伤。HVT在酸滴入后引起VILI,但在脓毒症期间不引起VILI。然而,这种不同的影响并没有观察到在系统释放的介体。
To examine whether acute lung injury from direct and indirect origins differ in susceptibility to ventilator-induced lung injury (VILI) and resultant systemic inflammatory responses. Rats were challenged by acid instillation or 24 h of sepsis induced by cecal ligation and puncture, followed by mechanical ventilation (MV) with either a low tidal volume (Vt) of 6 mL/kg and 5 cm H2O positive end-expiratory pressure (PEEP; LVt acid, LVt sepsis) or with a high Vt of 15 mL/kg and no PEEP (HVt acid, HVt sepsis). Rats sacrificed immediately after acid instillation and non-ventilated septic animals served as controls. Hemodynamic and respiratory variables were monitored. After 4 h, lung wet to dry (W/D) weight ratios, histological lung injury and plasma mediator concentrations were measured. Oxygenation and lung compliance decreased after acid instillation as compared to sepsis. Additionally, W/D weight ratios and histological lung injury scores increased after acid instillation as compared to sepsis. MV increased W/D weight ratio and lung injury score, however this effect was mainly attributable to HVt ventilation after acid instillation. Similarly, effects of HVt on oxygenation were only observed after acid instillation. HVt during sepsis did not further affect oxygenation, compliance, W/D weight ratio or lung injury score. Plasma interleukin-6 and tumour necrosis factor-α concentrations were increased after acid instillation as compared to sepsis, but plasma intercellular adhesion molecule-1 concentration increased during sepsis only. In contrast to lung injury parameters, no additional effects of HVt MV after acid instillation on plasma mediator concentrations were observed. During MV more severe lung injury develops after acid instillation as compared to sepsis. HVt causes VILI after acid instillation, but not during sepsis. However, this differential effect was not observed in the systemic release of mediators.
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