Aslan A, Karagüzel G, Gura A, Karaveli C, Bulbul M, Melikoglu M
Department of Pediatric Surgery, Akdeniz University School of Medicine, 07070 Antalya, Turkey.
Eur J Pediatr Surg. 2006 Oct;16(5):307-11. doi: 10.1055/s-2006-924638.
Experiential studies suggest that re-expansion of a collapsed lung may result in pulmonary ischaemia-reperfusion injury. We aimed to evaluate the effect of lung re-expansion on urinary lipid peroxidation products in neonates with pneumothorax.
This study included 20 mechanically ventilated neonates with pneumothorax, and 18 healthy neonates (controls). A chest tube was inserted immediately following the diagnosis of pneumothorax. Urine samples were obtained just before tube thoracostomy (first period), after one hour (second period), every 12 hours by complete reexpansion (third period). Vital signs and ventilatory parameters were recorded. Urinary lipid peroxidation was evaluated by measurement of thiobarbituric acid-reacting substances (TBARS).
No significant difference was found between urinary TBARS concentrations in the first, second and third periods (4.08 +/- 2.4 nmol/L, 2.8 +/- 2.3 nmol/L and 3.3 +/- 2.1 nmol/L, respectively). Control TBARS levels (4.1 +/- 2.1 nmol/L) did not significantly differ from those of the neonates with pneumothorax (p > 0.05). The neonates with pneumothorax had higher heart rates compared to the controls (p < 0.01). When compared with controls, the systolic pressure was lower in all periods (p < 0.01), and diastolic blood pressure was lower only in the first and second period (p < 0.05). Oxygen saturation significantly decreased in the first period compared to saturation of the second period and of controls (p < 0.01). Ventilatory parameters did not show any significant difference between the periods.
This prospective study showed that re-expansion of the lung did not significantly affect urinary TBARS concentration in neonatal pneumothorax. Indirectly, short-term lung collapse followed by re-expansion might not cause a clinically significant reperfusion injury in newborns.
经验性研究表明,萎陷肺的重新扩张可能导致肺缺血-再灌注损伤。我们旨在评估肺重新扩张对气胸新生儿尿脂质过氧化产物的影响。
本研究纳入20例机械通气的气胸新生儿和18例健康新生儿(对照组)。气胸诊断后立即插入胸腔引流管。在胸腔闭式引流术前(第一阶段)、术后1小时(第二阶段)、完全复张后每12小时(第三阶段)采集尿样。记录生命体征和通气参数。通过测量硫代巴比妥酸反应物质(TBARS)评估尿脂质过氧化。
第一、第二和第三阶段尿TBARS浓度之间无显著差异(分别为4.08±2.4 nmol/L、2.8±2.3 nmol/L和3.3±2.1 nmol/L)。对照组的TBARS水平(4.1±2.1 nmol/L)与气胸新生儿的TBARS水平无显著差异(p>0.05)。气胸新生儿的心率高于对照组(p<0.01)。与对照组相比,各阶段收缩压均较低(p<0.01),舒张压仅在第一和第二阶段较低(p<0.05)。与第二阶段及对照组的饱和度相比,第一阶段氧饱和度显著降低(p<0.01)。各阶段通气参数无显著差异。
这项前瞻性研究表明,肺重新扩张对新生儿气胸尿TBARS浓度无显著影响。间接表明,短期肺萎陷后再扩张可能不会在新生儿中引起具有临床意义的再灌注损伤。