Cabrera-Aguilera Ignacio, Benito Begoña, Tajes Marta, Farré Ramon, Gozal David, Almendros Isaac, Farré Nuria
Unitat de Biofísica i Bioenginyeria, Facultat de Medicina i Ciències de la Salut, Universitat de Barcelona, Barcelona, Spain.
Departament of Human Movement Sciences, Faculty of Health Sciences, School of Kinesiology, Universidad de Talca, Talca, Chile.
Front Neurol. 2020 Jan 9;10:1364. doi: 10.3389/fneur.2019.01364. eCollection 2019.
Obstructive sleep apnea (OSA) has been associated with heart failure (HF). Sleep fragmentation (SF), one of the main hallmarks of OSA, induces systemic inflammation, oxidative stress and sympathetic activation, hence potentially participating in OSA-induced cardiovascular consequences. However, whether SF is deleterious to heart function is unknown. The aim of this study was to non-invasively evaluate the effect of SF mimicking OSA on heart function in healthy mice and in mice with HF. Forty C57BL/6J male mice were randomized into 4 groups: control sleep (C), sleep fragmentation (SF), isoproterenol-induced heart failure (HF), and mice subjected to both SF+HF. Echocardiography was performed at baseline and after 30 days to evaluate left ventricular end-diastolic (LVEDD) and end-systolic (LVESD) diameters, left ventricular ejection fraction (LVEF) and fraction shortening (FS). The effects of SF and HF on these parameters were assessed by two-way ANOVA. Mice with isoproterenol-induced HF had significant increases in LVEDD and LVESD, as well as a decreases in LVEF and FS ( = 0.013, = 0.006, = 0.027, and = 0.047, respectively). However, no significant effects emerged with SF ( = 0.480, = 0.542, = 0.188, and = 0.289, respectively). Chronic SF mimicking OSA did not induce echocardiographic changes in cardiac structure and function in both healthy and HF mice. Thus, the deleterious cardiac consequences of OSA are likely induced by other perturbations associated with this prevalent condition, or result from interactions with underlying comorbidities in OSA patients.
阻塞性睡眠呼吸暂停（OSA）与心力衰竭（HF）有关。睡眠片段化（SF）是OSA的主要特征之一，可诱发全身炎症、氧化应激和交感神经激活，因此可能参与OSA引起的心血管后果。然而，SF是否对心脏功能有害尚不清楚。本研究的目的是无创评估模拟OSA的SF对健康小鼠和HF小鼠心脏功能的影响。40只C57BL/6J雄性小鼠被随机分为4组：对照睡眠（C）组、睡眠片段化（SF）组、异丙肾上腺素诱导的心力衰竭（HF）组和同时接受SF+HF的小鼠组。在基线和30天后进行超声心动图检查，以评估左心室舒张末期（LVEDD）和收缩末期（LVESD）直径、左心室射血分数（LVEF）和缩短分数（FS）。通过双向方差分析评估SF和HF对这些参数的影响。异丙肾上腺素诱导的HF小鼠的LVEDD和LVESD显著增加，LVEF和FS降低（分别为P = 0.013、P = 0.006、P = 0.027和P = 0.047）。然而，SF对这些参数没有显著影响（分别为P = 0.480、P = 0.542、P = 0.188和P = 0.289）。模拟OSA的慢性SF在健康小鼠和HF小鼠中均未引起心脏结构和功能的超声心动图改变。因此，OSA的有害心脏后果可能是由与这种常见疾病相关的其他干扰因素引起的，或者是由与OSA患者潜在合并症的相互作用导致的。
