Lazarov Simeon, Yanev Emil, Momchilova Albena, Markovska Tania, Ivanova Lidia, Pankov Roumen
Department of Pathophysiology, Medical University, 1431 Sofia, Bulgaria.
Chem Biol Interact. 2007 Aug 30;169(2):73-9. doi: 10.1016/j.cbi.2007.05.005. Epub 2007 May 24.
Pulmonary complications often accompany the development of acute peritonitis. In this study, we analyzed the alterations of alveolar surfactant phospholipids in rats with experimentally induced peritonitis. The results showed a reduction of almost all phospholipid fractions in pulmonary surfactant of experimental animals. The most abundant alveolar phospholipids-phosphatidylcholine and phosphatidylglycerol were reduced significantly in surfactant of rats with experimental peritonitis. In addition, analysis of the fatty acid composition of these two phospholipids revealed marked differences between experimental and control animals. The activity of phospholipase A2, which is localized in the hydrophyllic phase of alveolar surfactant, was higher in rats with experimental peritonitis compared to sham-operated ones. Also, a weak acyl-CoA:lysophospholipid acyltransferase activity was detected in alveolar surfactant of rats with experimental peritonitis, whereas in control animals this activity was not detectable. The lipid-transfer activity was quite similar in pulmonary surfactant of control and experimental rats. The total number of cells and the percentage of neutrophils were strongly increased in broncho-alveolar lavage fluid from rats with peritonitis. Thus, our results showed that the development of peritonitis was accompanied by pulmonary pathophysiological processes that involved alterations of the phospholipid and fatty acid composition of alveolar surfactant. We suggest that the increased populations of inflammatory cells, which basically participate in internalization and secretion of surfactant components, contributed to the observed alterations of alveolar phospholipids. These studies would be useful for clarification of the pathogenic mechanisms underlying the occurrence of pulmonary disorders that accompany acute inflammatory conditions, such as peritonitis and sepsis.
肺部并发症常伴随急性腹膜炎的发生。在本研究中,我们分析了实验性诱导腹膜炎大鼠肺泡表面活性物质磷脂的变化。结果显示,实验动物肺表面活性物质中几乎所有磷脂组分均减少。实验性腹膜炎大鼠表面活性物质中最丰富的肺泡磷脂——磷脂酰胆碱和磷脂酰甘油显著减少。此外,对这两种磷脂脂肪酸组成的分析揭示了实验动物与对照动物之间的显著差异。定位于肺泡表面活性物质亲水相的磷脂酶A2活性,在实验性腹膜炎大鼠中高于假手术大鼠。而且,在实验性腹膜炎大鼠的肺泡表面活性物质中检测到较弱的酰基辅酶A:溶血磷脂酰基转移酶活性,而在对照动物中未检测到该活性。对照大鼠和实验大鼠肺表面活性物质中的脂质转运活性相当相似。腹膜炎大鼠支气管肺泡灌洗液中的细胞总数和中性粒细胞百分比显著增加。因此,我们的结果表明,腹膜炎的发生伴随着肺部病理生理过程,这些过程涉及肺泡表面活性物质磷脂和脂肪酸组成的改变。我们认为,基本上参与表面活性物质成分内化和分泌的炎症细胞数量增加,导致了观察到的肺泡磷脂改变。这些研究将有助于阐明伴随急性炎症性疾病(如腹膜炎和败血症)发生的肺部疾病的发病机制。