Inflammation status of rabbit carotid artery model endothelium during intermittent hypoxia exposure and its relationship with leptin

Abstract

IH/ROX activated the inflammation pathway significantly in the endothelium, which was more intensive than CH and intensity-dependent. When exposed to both IH/ROX and leptin, inflammation occurs more dramatically. It means that synergic activating roles were performed by IH/ROX and leptin. This study may have a clinical implication that IH can cause endothelial damage through activated inflammation in OSA patients, and if the OSA patients have obesity at the same time, the endothelial damage or the inflammation would be more significant because of elevated leptin level as a synergic factor.

Systematic and Endothelial Inflammation and Endothelial Progenitor Cell Levels in Emphysematous Rats Exposed to Intermittent Hypoxia

“…26 Activated RhoA shrinks endothelial cells and increases cell permeability, making it more feasible for inflammatory cells, like leukocytes, to pass through the endothelial barrier when it combines with elevated adhesive capability caused by cellular inflammation. 6 One of our previous studies suggests that IH may cause endothelial damage through activated IL-6 and RhoA in OSA patients. 6 Moreover, in another study, it has been demonstrated that the RhoA, with its downstream effector Rho kinase, has been involved in systematic endothelial dysfunction in smokers with normal lung function.…”

“…6 One of our previous studies suggests that IH may cause endothelial damage through activated IL-6 and RhoA in OSA patients. 6 Moreover, in another study, it has been demonstrated that the RhoA, with its downstream effector Rho kinase, has been involved in systematic endothelial dysfunction in smokers with normal lung function. The authors found GTP-RhoA protein expression was significantly increased in patients with COPD.…”

“…We used an IH exposure device similar to those used in our previous studies. 6,8 Briefly, a gas control delivery system was designed to regulate the flow (5 L/min) of nitrogen (N 2 , IH phase) or clean air (air, normoxia phase) alternatively into a customized IH housing chamber (23 cm ϫ 20 cm ϫ 12 cm ϭ 5,520 cm 3 Ϸ 5.5 L) to maintain a designated IH or normoxia environment. A series of programmable solenoids and flow regulators altered the fractional concentration of inspired oxygen that controlled the durations of hypoxia (30 s) or normoxia phase (90 s) and produced 30 cycles of alternations/h, and the nadir oxygen concentration in the IH housing chamber was approximately 5%.…”

“…Optical density values of reverse transcription polymerase chain reaction results were standardized with the results of the control group. 6 …”

“…These approaches simplify the research process and attain most of the academic goals. [5][6][7][8][9] Cardiovascular diseases represent a major comorbidity in each disorder of OS. Both COPD and OSA are associated with increased activation of many inflammatory cells and molecular mechanisms associated with atherosclerosis, which provide basic mechanisms to support the clinical and epidemiological data demonstrating COPD and OSA as independent risk factors for cardiovascular diseases.…”