Endothelial dysfunction in emphysematous rats exposed to intermittent hypoxia and interventional effects of tempol

Aim: We developed an overlap syndrome rat model of intermittent hypoxia based of emphysema exposure to explore whether OS can lead to more severe vascular endothelial injury and to assess the intervention effects of tempol. Methods: Male Wistar rats (n=60)were randomly distributed into 6 groups: normal oxygen control (NC), intermittent hypoxia (IH), continuous hypoxia (CH), exposure to smoke and IH (OS), exposure to OS and treated with tempol (OST), exposure to OS and treated with NaCl (OSN). After an 8-week challenge, lung tissues were stained with hematoxylin/eosin (H/E). The level of intracellular adhesion molecule-1 (ICAM-1) and vascular cellular adhesion molecule-1 (VCAM-1) were detected by enzyme-linked immunosorbent assay (ELISA), and the apoptosis of circulating endothelial cells (CECs) were analysed by flow cytometry. Results: The pathological changes in the lungs of the CH group were the formation of emphysema accompanied by infiltration of inflammatory cells, the partial fracture of the bronchial wall smooth muscle, and goblet cell hyperplasia, which were more severe in the OS group. The levels of ICAM-1, VCAM-1 and CEC apoptosis were highest in the OS group and lowest in the NC group. Administration of tempol in OS rats significantly reduced the levels described above compared with the non-tempol-treated group. Conclusion: Overlap syndrome-related inflammation and endothelial cell apoptosis may play important roles by promoting cardiovascular dysfunction and CVD. When IH is combined with emphysema, synergistic effects appear, and produce a more significant inflammatory status and endothelial injury. It is important that tempol treatment attenuated this effect