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Roles of pulmonary vascular endothelial cell injury and dimethylargininedimethylaminohydrolase/nitric oxide synthase/nitric oxide-system changes in the occurrence of diabetic sepsis in rats

Xiujuan Liu, Fuzai Yin, Kun Wei, Yue Zheng, Lanxiang Liu, Fang Qiu, Yonghong Xie, Shufeng Xu, En Mu, Yingjian Liang, Zhidan Zhang, Xiaochun Ma

The aim of this study was to investigate the roles of Pulmonary Microvascular Endothelial Cell Injury (PMECI) and Nitric Oxide (NO) system in diabetic sepsis in rats. 64 Wistar rats were randomly divided into group A (the normal control group), group B (the sepsis group), group C (the diabetes group), and group D (the diabetic sepsis group), the content of pulmonary Evans blue (EBD) was measured; the pulmonary microvascular permeability was observed; specific Tyrosine kinase receptor 2 (Tie-2) mRNA in whole blood was measured by Polymerase Chain Reaction (PCR) assay to understand the amount of endothelial cells in the circulation; the content of NO in serum/lung tissues, as well as the content of inducible Nitric Oxide Synthase (iNOS) mRNA/endothelial Nitric Oxide Synthase (eNOS) mRNA in lung tissues, were detected to observe the roles of NO system. The EBD content in group D was the highest, followed by group B, and exhibited statistical difference than group A and C (P<0.01); Tie-2 mRNA in group D was significantly increased than the other three groups (P<0.01); the NO contents in the serum and lung tissues of group B/D were higher than the other two groups. The iNOS mRNA content in group D was the highest, while that of eNOS mRNA was the lowest, and the differences were statistically significant (P<0.05). Diabetes associated with sepsis might aggravate endothelial cell injury, and it was considered to be related with the imbalanced adjustments of the NO system.