This study investigated the effects of acute hypobaric hypoxia at high altitude on cardiac function and the expression of miR-144 in myocardium in rats.

Adult male Sprague-Dawley rats were randomly assigned to a normoxic group and four hypoxic groups (HH group). Rats in hypoxic groups were exposed to simulated hypobaric hypoxia chamber equivalent to 7 000 meters for different durations (3, 7, 14 and 28 days). Subsequently, echocardiography was used to detect cardiac structure and function in rats. QRT-PCR was used to detect the expression of miR-144 in myocardium of rats.

Compared with the normoxic group, both LVEF and FS decreased in HH3 and HH7 group, both LVEF and FS increased in HH14 and HH28 group. Both PV peak velocity and PV peak gradient in all hypoxic groups were lower than those in normoxic group. Both LVIDD and LVIDS in all hypoxic groups were shorter than those in normoxic group. The LVPWD were thicker in all hypoxic groups than that in normoxic group. The expression of miR-144 in myocardium in HH3, HH7 and HH28 group were higher than that in normoxic group. The expression of miR-144 in myocardium in HH14 group was lower slightly than that in normoxic group. Spearman correlation analysis showed that the expression of miR-144 was negatively correlated with left ventricular ejection fraction and short axis shortening rate.

Acute hypobaric hypoxia at high altitude can lead to changes of cardiac structure and function in rats. The left ventricular diameter decreased, the wall thickened, and the diastolic function decreased in rats by high altitude hypobaric hypoxia. Left ventricular systolic function increased during one week by high altitude hypobaric hypoxia, but recovered then. Acute hypobaric hypoxia at high altitude could increase the expression of miR-144 in myocardium. The expression of miR-144 in myocardium was negatively correlated with LVEF and FS. It was possible that miR-144 could regulate cardiac function at high altitude hypobaric hypoxia.