The Study Of Chronic Intermittent Hypoxia Caused By Obstructive Sleep Apnea To The Rat Myocardial Cell Apoptosis And Myocardial Fibrosis

Background Sleep apnea patients appear repeatedly hypoxemia, hypercapnia, and structure of sleep disorders in the night, and relapse of intermittent hypoxia caused by hypoxia gave rise to a serious damage to the cardiovascular system, a large number of animal experiments and clinical observations show that sleep apnea can lead to high blood pressure, chronic intermittent hypoxia, the stimulation of chemical sensors, the activation of the sympathetic and the renin angiotensin system, and all of these affections may promote myocardial cell apoptosis and myocardial fibrosis, and aggravate cardiovascular disease. But how to influence the myocardial cell apoptosis and myocardial fibrosis by chronic intermittent hypoxia is not known.Objective The study of chronic intermittent hypoxia caused by obstructive sleep apnea to the rat myocardial cell apoptosis and myocardial fibrosis.Methods (1) Rats were randomly divided into chronic intermittent hypoxia group (CIH) and control group (NC):chronic intermittent hypoxia rats group (CIH) were risen into plexiglass chambers which were supplied by chronic intermittent hypoxia in 8 hours a day, and NC rats were placed in the same tank but as normal oxygen concentration environment. (2) Using echocardiography to determine left ventricular end-diastolic diameter (LVIDd), left ventricular end systolic diameter (LVIDs), left ventricular short axis shortening rate (LVFS) and left ventricular ejection fraction (LVEF) till the rats were raised at the end of the 35th day. (3) We selected samples to stain with HE, withTUNEL and with Picric acid-Sirius, then we detected the differences in myocardial structure, in myocardial apoptosis, and in the levels of myocardial fibrosis. (4)The myocardial protein was extracted to detect by Western blot comparing the expression level of HIF-1α protein. (5) The data were analysed by Spss 13.0. A p value less than 0.05 was considered statistically significant.Results (1) Compared with NC group, the rats of CIH group’s left ventricles were dilated with expanded left ventricular internal diameter in systole (LVIDs) [4.094+ 1.131 mm(CIH) versus 3.060±0.923mm (NC), p< 0.01], while left ventricular short axis shortening rate (LVFS) [38.127±11.564%(ClH) versus 51.170±12.425% (NC), p<0.01)]and left ventricular ejection fraction (LVEF) [74.247±10.345% (CIH) versus 87.290±9.436% (NC), p< 0.01]were both significantly reduced in CIH rats. (2) In CIH group, HE staining presented that myocardial cells were injured. Myocardial cell edema and part of cells necrobiosis appeared. The TUNEL positive apoptotic cells were markedly increased in the cardiac tissues of CIH-treated rats compared to control rats. Sirius staining showed a significant amount of collagen fibers in the heart of CIH rats.(3)The expression level of HIF-1α was markedly increased in the cardiac tissue of CIH rats compared to control rats by using Western blot test [0.62±2.89E-0.5 (CIH) versus 0.45±0.01 (NC), P<0.05].Conclusions (1) CIH caused cardiac dysfunction. (2) CIH induced cardiac injuries and fibrosis. (3) CIH activated hypoxia inducible factor-1α responses.