Abstract: Objective To explore the underlying molecular mechanisms relevant to intermittent hypoxia, remodeling and heart failure by observing the changes of remodeling, hemodynamic parameters, apoptosis and the expression of Rho kinase in the myocardial cells of rats with sleep intermittent hypoxia. Methods Male Wistar rats were given limited normal diet (20g/d per rat) and swam for 1hour at 6pm. The rats were divided into 3 groups (EM>n/EM>=8 per group): a normal oxygen group (group A, breathing 21% O2 for 8hours per day), an intermittent hypoxia group (group B, breathing 10% O2 and air altered per 90 sec for 8hours per day) and a fasudil group ［group C, breathing 10% O2 and air altered per 90 sec for 8hours per day, 20mg/(kgI>&#/I>8226;d) fasudil Qd, i.h.］. Sixty days later, hemodynamic parameters, left ventricular weight and weight of rats were measured. Morphological changes (HE staining), apoptosis and the expression of Rho kinase mRNA in rat myocardial cells were examined. Results As compared to group A, group B showed abnormal hemodynamic parameters, an increase in the index of left ventricular hypertrophy, disarrangement of myocardial cells, remarkable apoptosis, up-regulation of Rho kinase mRNA expression. These changes were improved significantly in group C in comparison with group B. Conclusion Intermittent hypoxia is associated with the pathogenesis of remodeling and heart failure. Apoptosis and Rho kinase may play a key role in remodel

Key words: Intermittent hypoxia, Ventricular remodeling, Rho kinase, Sleep apnea syndrome, RT-PCR, Rat