Abstract
A high-fat diet (HFD) accumulates fat in the cardiovascular system, alters the metabolism, and affects cardiac function. Dyslipidemia is associated with the development of sleep apnea syndrome (SAS), which is associated with intermittent hypoxia (IH); however, it is unclear whether SAS affects cardiac function in patients with dyslipidemia. The purpose of this study was to evaluate how IH affects cardiac function in rats fed with a HFD. Male 5-week-old Sprague-Dawley rats of two groups (normal diet (SD) and HFD) were divided into IH-exposed and unexposed groups. Zinc protoporphyrin-9 (ZnPPIX) was administered as a heme oxygenase-1 (HO-1) inhibitor to the SD and IH + HFD groups, and cardiac function and blood viscosity were examined. In the IH + HFD group, echocardiography showed an increased fractional shortening (FS), which peaked on day 4. Western blot analysis revealed an increase in HO-1 after 2 weeks. This peak continued even after the HO-1 inhibitor and ZnPPIX were administered. One cause of increased FS is the stagnation of blood flow due to an increased blood viscosity. To be able to send highly viscous blood to every corner of the body, the heart must contract strongly. Therefore, HO-1 is released by the body as a biological defense reaction. HO-1 has a vasodilatory effect and suppresses hyper constriction. Thus, IH exposure to HFD causes and drives transient hyper constriction, releasing HO-1 as a biological response. This led to dilated blood vessels, after which the FS returned to normal.