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STUDY OF PULMONARY SURFACTANT AND SURFACTANT PROTEIN IN RATS WITH LIPOPOLYSACCHARIDE-INDUCED ACUTE LUNG INJURY

Feng Xu, Yong He

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Abstract

INTRODUCTION: The abnormal metabolism of pulmonary surfactant (PS) may have some relationship to acute lung injury (ALI). OBJECTIVE: The objective of this study was to examine the alteration trend of PS and surfactant-associated protein (SP) in rats with lipopolysaccharide (LPS)-induced ALI. METHODS: Fifty-six adult Wistar rats were randomly divided into the normal saline (NS) group and the ALI group. The levels of mRNA of surfactant protein A (SP-A) and SP-B were measured by reverse-transcription polymerase chain reaction during intravenous LPS administration at 1, 3, 5, and 7 hours. The content and component of PS in the bronchoalveolar lavage fluid (BALF) were measured by high-performance liquid chromatography. In addition, lung dry/wet weight ratio, the protein content of BALF, alveolar oxygen partial pressure, and histologic changes were detected. RESULTS: Compared with the NS group, the ALI group developed severe lung damage; edema, hemorrhage, and inflammation were found. Total phospholipids in BALF at 1, 3, 5, and 7 hours were lower than those in the NS group; phosphatidylcholine at 3, 5, and 7 hours was lower than that in the NS group, whereas lysophosphatidylcholine at 1, 3, 5, and 7 hours was higher than that in the NS group. The expression of SP-A and SP-B mRNA at 3, 5, and 7 hours was less than that in the NS group. CONCLUSIONS: The changed metabolism of PS may be responsible for the pathogenesis of ALI. It is mainly demonstrated by the decrease in total phospholipids and phosphatidylcholine and the decreased expression of SP-A and SP-B mRNA. Decrease in content and change in components of PS may play an important role in severe hypoxemia in ALI.

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INTRODUCTION: The abnormal metabolism of pulmonary surfactant (PS) may have some relationship to acute lung injury (ALI). OBJECTIVE: The objective of this study was to examine the alteration trend of PS and surfactant-associated protein (SP) in rats with lipopolysaccharide (LPS)-induced ALI. METHODS: Fifty-six adult Wistar rats were randomly divided into the normal saline (NS) group and the ALI group. The levels of mRNA of surfactant protein A (SP-A) and SP-B were measured by reverse-transcription polymerase chain reaction during intravenous LPS administration at 1, 3, 5, and 7 hours. The content and component of PS in the bronchoalveolar lavage fluid (BALF) were measured by high-performance liquid chromatography. In addition, lung dry/wet weight ratio, the protein content of BALF, alveolar oxygen partial pressure, and histologic changes were detected. RESULTS: Compared with the NS group, the ALI group developed severe lung damage; edema, hemorrhage, and inflammation were found. Total phospholipids in BALF at 1, 3, 5, and 7 hours were lower than those in the NS group; phosphatidylcholine at 3, 5, and 7 hours was lower than that in the NS group, whereas lysophosphatidylcholine at 1, 3, 5, and 7 hours was higher than that in the NS group. The expression of SP-A and SP-B mRNA at 3, 5, and 7 hours was less than that in the NS group. CONCLUSIONS: The changed metabolism of PS may be responsible for the pathogenesis of ALI. It is mainly demonstrated by the decrease in total phospholipids and phosphatidylcholine and the decreased expression of SP-A and SP-B mRNA. Decrease in content and change in components of PS may play an important role in severe hypoxemia in ALI.

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Available abstract

INTRODUCTION: The abnormal metabolism of pulmonary surfactant (PS) may have some relationship to acute lung injury (ALI). OBJECTIVE: The objective of this study was to examine the alteration trend of PS and surfactant-associated protein (SP) in rats with lipopolysaccharide (LPS)-induced ALI. METHODS: Fifty-six adult Wistar rats were randomly divided into the normal saline (NS) group and the ALI group. The levels of mRNA of surfactant protein A (SP-A) and SP-B were measured by reverse-transcription polymerase chain reaction during intravenous LPS administration at 1, 3, 5, and 7 hours. The content and component of PS in the bronchoalveolar lavage fluid (BALF) were measured by high-performance liquid chromatography. In addition, lung dry/wet weight ratio, the protein content of BALF, alveolar oxygen partial pressure, and histologic changes were detected. RESULTS: Compared with the NS group, the ALI group developed severe lung damage; edema, hemorrhage, and inflammation were found. Total phospholipids in BALF at 1, 3, 5, and 7 hours were lower than those in the NS group; phosphatidylcholine at 3, 5, and 7 hours was lower than that in the NS group, whereas lysophosphatidylcholine at 1, 3, 5, and 7 hours was higher than that in the NS group. The expression of SP-A and SP-B mRNA at 3, 5, and 7 hours was less than that in the NS group. CONCLUSIONS: The changed metabolism of PS may be responsible for the pathogenesis of ALI. It is mainly demonstrated by the decrease in total phospholipids and phosphatidylcholine and the decreased expression of SP-A and SP-B mRNA. Decrease in content and change in components of PS may play an important role in severe hypoxemia in ALI.

Key concepts: Medicine, Bronchoalveolar lavage, Pulmonary surfactant, Lysophosphatidylcholine, Lung, Lipopolysaccharide, Phosphatidylcholine, Pulmonary edema

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