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Meconium aspiration induces ARDS-like pulmonary response in lungs of ten-week-old pigs.

机译:胎粪吸入会在十周龄的猪的肺中诱发类似ARDS的肺反应。

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To investigate whether aspiration of meconium induces a hemodynamic and histologic pulmonary response similar to that frequently seen in experimental acute respiratory distress syndrome, twelve 10-week-old pigs with postnatally adapted lungs were studied. Six 10-week-old pigs received 3 ml/kg 20% human meconium via the endotracheal tube. Six control pigs of the same age were given sterile saline. Ventilator settings were adjusted to keep PaO2 above 8 kPa and PaCO2 below 5 kPa. The pulmonary hemodynamic response to aspiration consisted of two separate hypertensive components. An initial peak in pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) was followed by a progressive increase in PAP and PVR in the meconium group, whereas in the saline group these parameters returned to baseline levels. The distribution of PVR, determined by pulmonary artery occlusion, was characterized by an increase in the postarterial resistance immediately after meconium aspiration and a progressive increase in both arterial and postarterial resistance during the later phase. On histological examination, marked neutrophil sequestration was seen in the meconium lungs. In addition, lung edema formation was significantly enhanced in the meconium group, as shown by an increased lung wet/dry weight ratio. Thus, meconium aspiration resulted in a biphasic pulmonary pressor response and severe pulmonary inflammation. This response resembled that of models of experimental acute respiratory distress syndrome following diverse types of precipitating insults; this suggests that similar pathophysiologic mechanisms are elicited and cause similar pulmonary dysfunction following different forms of lung injury.
机译:为了研究粪便吸入是否引起类似于在实验性急性呼吸窘迫综合征中常见的血液动力学和组织学肺部反应,研究了十二只10周大的具有出生后适应性肺的猪。六只10周龄的猪通过气管导管接受了3 ml / kg 20%的人胎粪。给六只相同年龄的对照猪提供无菌盐水。调整呼吸机设置,以使PaO2保持在8 kPa以上,PaCO2保持在5 kPa以下。肺对抽吸的血液动力学反应由两个独立的高血压成分组成。胎粪组的肺动脉压(PAP)和肺血管阻力(PVR)最初达到峰值,然后PAP和PVR逐渐升高,而在盐水组中,这些参数恢复到基线水平。 PVR的分布由肺动脉闭塞决定,其特征是胎粪吸入后立即增加了动脉后阻力,并在随后的阶段逐渐增加了动脉和动脉后阻力。在组织学检查中,在胎粪肺中观察到明显的中性白细胞隔离。另外,在胎粪组中,肺水肿的形成显着增强,如肺湿重/干重比的增加所表明。因此,胎粪吸入导致双相肺升压反应和严重的肺部炎症。这种反应类似于对各种类型的沉淀性损伤后的实验性急性呼吸窘迫综合征模型的反应。这表明,在不同形式的肺损伤后,会引起相似的病理生理机制并引起相似的肺功能障碍。

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