Department of Orthodontics, School and Hospital of Stomatology, Hebei Medical University & Hebei Key Laboratory of Stomatology, Shijiazhuang, 050017, P.R. China.
Department of Periodontology and Dental Hygiene, School of Dentistry, University of Detroit Mercy, Detroit, MI, USA.
Sci Rep. 2020 Feb 25;10(1):3394. doi: 10.1038/s41598-020-60034-1.
Although considerable research highlights the interactions between obstructive sleep apnea-hypopnea syndrome (OSAHS) and cardiovascular diseases, the effect of mandibular advancement device (MAD) treatment on cardiovascular complications in OSAHS patients remains unclear. We evaluated the effect of OSAHS treatment with MADs on the myocardium. All methods in this study were in accordance with relevant guidelines and regulations of the medical ethics committee in Hospital of Stomatology, Hebei Medical University approved the work. Thirty New Zealand rabbits were randomized into three groups: the control group, Group OSAHS, and Group MAD. Hydrophilic polyacrylamide gel was injected into the soft palate of the rabbits to induce OSAHS. In Group MAD, a MAD was positioned after OSAHS induction. All animals were induced to sleep in a supine position for 4-6 h/day for 8 weeks. Echocardiography was used to determine the structure and function of the heart. The histological changes were detected by optical microscopy and transmission electron microscopy (TEM). The levels of ET-1(endothelin-1) and Ang II (Angiotensin II) in the plasma were measured by an enzyme-linked immunosorbent assay (ELISA). The expression of ET-1 mRNA in heart tissue was detected by RT-PCR. Histological abnormalities, left ventricular hypertrophy, and left ventricular dysfunctions were demonstrated in Group OSAHS, and the abnormities were rescued with MAD treatment. Higher levels of plasma ET-1 and Ang II and elevated expression of ET-1 mRNA in cardiac tissue were detected in Group OSAHS compared with Group MAD and the control group. The blood oxygen saturation was negatively correlated with the levels of ET-1 and Ang II. OSAHS-induced elevated levels of ET-1 and Ang II may be attributed to myocardial structural abnormalities and dysfunction. Early treatment of MADs may play an important role in preventing myocardial damage in OSAHS rabbit model.
尽管大量研究强调了阻塞性睡眠呼吸暂停低通气综合征（OSAHS）与心血管疾病之间的相互作用，但下颌前伸装置（MAD）治疗对 OSAHS 患者心血管并发症的影响仍不清楚。我们评估了 MAD 治疗 OSAHS 对心肌的影响。本研究中的所有方法均符合河北医科大学口腔医院医学伦理委员会的相关指南和规定，该工作得到了委员会的批准。30 只新西兰兔随机分为三组：对照组、OSAHS 组和 MAD 组。向兔软腭内注射亲水性聚丙烯酰胺凝胶以诱导 OSAHS。在 MAD 组，在诱导 OSAHS 后放置 MAD。所有动物均在仰卧位诱导睡眠，每天 4-6 小时，持续 8 周。使用超声心动图确定心脏的结构和功能。光学显微镜和透射电子显微镜（TEM）检测组织学变化。通过酶联免疫吸附试验（ELISA）测量血浆中 ET-1（内皮素-1）和 Ang II（血管紧张素 II）的水平。通过 RT-PCR 检测心脏组织中 ET-1 mRNA 的表达。OSAHS 组出现组织学异常、左心室肥厚和左心室功能障碍，MAD 治疗可挽救这些异常。与 MAD 组和对照组相比，OSAHS 组血浆 ET-1 和 Ang II 水平升高，心脏组织中 ET-1 mRNA 表达升高。血氧饱和度与 ET-1 和 Ang II 水平呈负相关。OSAHS 诱导的 ET-1 和 Ang II 水平升高可能与心肌结构异常和功能障碍有关。早期 MAD 治疗可能在预防 OSAHS 兔模型心肌损伤中发挥重要作用。
