GW24-e3535 Obstructive sleep apnea syndrome and myocardium β receptor expression for empirical study

Objectives This experiment is to observe the chronic obstructive sleep apnea syndrome (OSAS) in dogs with the influence of cardiac structural remodelling and function,to discuss dog β-adrenergic receptor (β-AR) expression level change in the ventricular muscle of OSAS, for further study on the ventricular muscle influence OSAS provides theoretical basis. Methods 1) 14 dogs were randomly divided into normal group (n = 7) and OSAS group (n = 7). Under aseptic conditions, OSAS group do tracheal intubation after anaesthesia daily, and clamping tracheal intubation for 12 weeks to build chronic OSAS model. At the beginning of the two week, clamping the tracheal intubation 1 min every 9min, making apnea/ hypopnea index (AHI) is 6. Subsequently, decreasing interval time 1min every 1 week and maintaining AHI is 20 at last. Normal group is not gived airway obstruction intervention everyday. 2) The heart structure of dogs are measured by echocardiography. 3) Pathohistological and ultrastructural changes were tested by light microscope and transmission electron microscope. 4) The mRNA expression levels of β 1 -AR, β 2 -AR and β 3 -AR of the normal group and OSAS group were detected by RT-PCR experiments. Results 1) The heart ultrasound shows: the heart construction of OSAS group dog have been increased significantly compared with control group, LVEF has been reduced (p 1 -AR decreased in the RT-PCR experiments (p 2 -AR mRNA expression levels slightly decreased (p > 0.05) , and β 3 -AR mRNA expression levels increased (p Conclusions Ventricular structure is remodeled and function are also remodeled in the chronic obstructive sleep apnea. The mRNA of β 1 -AR expression levels decreased, the mRNA of β 2 -AR expression levels decreased, and the mRNA of β 3 -AR expression levels increased. This change may be relationship between OSAS associated cardiac structure and function changes, or with obstructive sleep apnea syndrome itself influence on β-AR expression level.