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首页> 外文期刊>Journal of Intensive Care >Adrenaline aggravates lung injury caused by liver ischemia–reperfusion and high-tidal-volume ventilation in rats
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Adrenaline aggravates lung injury caused by liver ischemia–reperfusion and high-tidal-volume ventilation in rats

机译:肾上腺素加重大鼠肝脏缺血再灌注和高潮气量通气引起的肺损伤

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BackgroundWe often administer adrenaline to improve hypotension of patients undergoing systemic inflammation that is not treated with volume resuscitation. The effects of adrenaline on injured lungs during shock status have not been elucidated. We previously demonstrated that hepatic ischemia–reperfusion followed by high-tidal-volume ventilation-induced systemic inflammation, hypotension, and lung injury in rats. Using this animal model, we investigated the effects of adrenaline on lung injury and hemodynamics. MethodsAnesthetized rats were ventilated and underwent hepatic inflow interruption for 15?min twice. After the second liver ischemia–reperfusion, the tidal volume was increased to 24?ml?·?kg?1 body weight from 6?ml?·?kg?1, and 12 rats in each group were observed for 360?min after reperfusion with or without continuous intravenous adrenaline administration. Extra fluid was administered according to the decline in the arterial blood pressure. ResultsAdrenaline administration significantly reduced the volume of intravenous resuscitation fluid. The wet-to-dry weight ratio of the lungs was higher (7.53?±?0.37 vs. 4.63?±?0.35, P 2.64?±?100.22 vs. 101.91?±?100.27, P =?0.015), with adrenaline. Histopathological examinations revealed marked exudation in the alveolar spaces in rats receiving adrenaline. ConclusionsContinuous administration of adrenaline partially prevented a rapid decline in blood pressure but deteriorated lung injury in a rat model of liver ischemia–reperfusion with high-tidal-volume ventilation. A possibility that adrenaline administration aggravate ventilator-induced lung injury during systemic inflammation should be considered.
机译:背景我们经常给予肾上腺素以改善未进行体积复苏的全身性炎症患者的低血压。尚未阐明在休克状态下肾上腺素对受伤的肺的影响。我们先前证明了肝脏缺血-再灌注继之以高潮气量通气引起的大鼠全身性炎症,低血压和肺损伤。使用这种动物模型,我们研究了肾上腺素对肺损伤和血液动力学的影响。方法将麻醉的大鼠通气,并中断肝入流两次,持续15分钟。第二次肝脏缺血再灌注后,潮气量从6?ml?·?kg ?1 增加到24?ml?·?kg ?1 体重,在有或没有连续静脉注射肾上腺素的情况下,在每组中的12只大鼠和再灌注后观察360分钟。根据动脉血压的下降给予额外的液体。结果肾上腺素给药显着减少了静脉复苏液的量。肺的干湿重比更高(7.53?±?0.37对4.63?±?0.35,P 2.64 ?±?10 0.22 对10 1.91 ?±?10 0.27 ,P =?0.015),带有肾上腺素。组织病理学检查显示,接受肾上腺素的大鼠的肺泡腔内明显渗出。结论在高潮气量通气的肝缺血再灌注大鼠模型中,连续给予肾上腺素可部分阻止血压的快速下降,但恶化了肺损伤。应考虑肾上腺素给药在全身性炎症期间加重呼吸机诱发的肺损伤的可能性。

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