R Wu1, X Song, Y Xu, X Meng. 1. Institute of General Surgery, General Hospital of People's Liberation Army, Beijing 100853, China.
Abstract
OBJECTIVE: To investigate the apoptosis of endothelial cells in the alteration of microvascular permeability in lung during sepsis. METHODS: Twenty-four male NIH mice were subjected to cecal ligation and puncture (CLP) or sham operation (SO). The microvascular endothelial cells of the lungs were harvested at 3 hours and 12 hours after operation. The apoptosis of endothelial cells (VIII factor related antigen positive cells) in the lungs was determined by 2-color flow cytometry (FITC-labeled VIII factor related antigen and PI) and Apop Tag) in situ apoptosis detection kit in situ. The apoptosis related gene (bcl-2) was detected by RT-PCR. The microvascular permeability in lung tissue was also examined. RESULTS: The apoptosis of microvascular endothelial cells was increased significantly at 12 hours after CLP (5.03 +/- 0.92 vs. 3.48 +/- 1.21, P < 0.05). The increased apoptosis was paralleled with the decrease in bcl-2 gene expression. The microvascular permeability in lung tissue was slightly increased at 3 hours after CLP, but significantly increased at 12 hours after CLP (0.106 +/- 0.008 vs 0.047 +/- 0.003, P < 0.01). CONCLUSIONS: Apoptosis in microvascular endothelial cells seems to be an important reason for the alteration of microvascular permeability.
OBJECTIVE: To investigate the apoptosis of endothelial cells in the alteration of microvascular permeability in lung during sepsis. METHODS: Twenty-four male NIH mice were subjected to cecal ligation and puncture (CLP) or sham operation (SO). The microvascular endothelial cells of the lungs were harvested at 3 hours and 12 hours after operation. The apoptosis of endothelial cells (VIII factor related antigen positive cells) in the lungs was determined by 2-color flow cytometry (FITC-labeled VIII factor related antigen and PI) and Apop Tag) in situ apoptosis detection kit in situ. The apoptosis related gene (bcl-2) was detected by RT-PCR. The microvascular permeability in lung tissue was also examined. RESULTS: The apoptosis of microvascular endothelial cells was increased significantly at 12 hours after CLP (5.03 +/- 0.92 vs. 3.48 +/- 1.21, P < 0.05). The increased apoptosis was paralleled with the decrease in bcl-2 gene expression. The microvascular permeability in lung tissue was slightly increased at 3 hours after CLP, but significantly increased at 12 hours after CLP (0.106 +/- 0.008 vs 0.047 +/- 0.003, P < 0.01). CONCLUSIONS: Apoptosis in microvascular endothelial cells seems to be an important reason for the alteration of microvascular permeability.