Mandibular Advancement Devices Prevent the Adverse Cardiac Effects of Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS)

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...

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Veröffentlicht in:Scientific reports 2020-02, Vol.10 (1), p.3394, Article 3394
Hauptverfasser: Liu, Chunyan, Kang, Wenjing, Zhang, Shilong, Qiao, Xing, Yang, Xiuchun, Zhou, Zheng, Lu, Haiyan
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Kang, Wenjing
Zhang, Shilong
Qiao, Xing
Yang, Xiuchun
Zhou, Zheng
Lu, Haiyan
description 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.
doi_str_mv 10.1038/s41598-020-60034-1
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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. 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Early treatment of MADs may play an important role in preventing myocardial damage in OSAHS rabbit model.</description><subject>101/28</subject><subject>13</subject><subject>13/21</subject><subject>14/63</subject><subject>38</subject><subject>38/22</subject><subject>45/22</subject><subject>631/337/572/2102</subject><subject>631/443/1784</subject><subject>631/535/1258/1259</subject><subject>82/80</subject><subject>96/21</subject><subject>Acrylic Resins - toxicity</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - blood</subject><subject>Animals</subject><subject>Apnea</subject><subject>Cardiovascular diseases</subject><subject>Cytokines - metabolism</subject><subject>Echocardiography</subject><subject>Endothelin 1</subject><subject>Endothelin-1 - blood</subject><subject>Endothelin-1 - genetics</subject><subject>Endothelin-1 - metabolism</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Gene expression</subject><subject>Heart</subject><subject>Heart - physiopathology</subject><subject>Humanities and Social Sciences</subject><subject>Hypertrophy</subject><subject>Light microscopy</subject><subject>Male</subject><subject>Mandible</subject><subject>Microscopy</subject><subject>mRNA</subject><subject>multidisciplinary</subject><subject>Myocardium</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Occlusal Splints</subject><subject>Palate</subject><subject>Polyacrylamide</subject><subject>Polymerase chain reaction</subject><subject>Polysomnography</subject><subject>Rabbits</subject><subject>RNA, Messenger - metabolism</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Sleep</subject><subject>Sleep apnea</subject><subject>Sleep Apnea, Obstructive - chemically induced</subject><subject>Sleep Apnea, Obstructive - therapy</subject><subject>Sleep disorders</subject><subject>Structure-function relationships</subject><subject>Transmission electron microscopy</subject><subject>Ventricle</subject><subject>Ventricular Dysfunction, Left - pathology</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU9P4zAQxS20CFCXL8ABWdrLcgjr-E9iX1aqCkuRQEUqnC3HGUOqNsnaSVC__bq0QPeCLx7rvXkz1g-hs5RcpoTJX4GnQsmEUJJkhDCepAfohBIuEsoo_bZXH6PTEBYkHkEVT9UROmaUKKlyfoJe701dVkW_NB6Py8HUFlZQd_gKhspCwA8ehs27e4GNDj4AnhhfVsbia-fAdgE3Ds-K0PnedtUAeL4EaPG4rcEk03XbbAo8X9elb1aAf87m4-n84js6dGYZ4HR3j9DTn-vHyTS5m93cTsZ3ieU57xLJjHEydyDLgvHC5oXJSOmIFEwK6tKMOMNEAQqkcraklEdBFcIolwnnFBuh39vcti9WUNr4F2-WuvXVyvi1bkyl_1fq6kU_N4POCadU0BjwYxfgm789hE4vmt7XcWdNWcaUkDnLo4tuXdY3IXhwHxNSoje89JaXjrz0Gy-dxqbz_d0-Wt7pRAPbGkKU6mfwn7O_iP0HMN2iOg</recordid><startdate>20200225</startdate><enddate>20200225</enddate><creator>Liu, Chunyan</creator><creator>Kang, Wenjing</creator><creator>Zhang, Shilong</creator><creator>Qiao, Xing</creator><creator>Yang, Xiuchun</creator><creator>Zhou, Zheng</creator><creator>Lu, Haiyan</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8891-5103</orcidid></search><sort><creationdate>20200225</creationdate><title>Mandibular Advancement Devices Prevent the Adverse Cardiac Effects of Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS)</title><author>Liu, Chunyan ; 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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.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32098974</pmid><doi>10.1038/s41598-020-60034-1</doi><orcidid>https://orcid.org/0000-0002-8891-5103</orcidid><oa>free_for_read</oa></addata></record>
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subjects 101/28
13
13/21
14/63
38
38/22
45/22
631/337/572/2102
631/443/1784
631/535/1258/1259
82/80
96/21
Acrylic Resins - toxicity
Angiotensin
Angiotensin II
Angiotensin II - blood
Animals
Apnea
Cardiovascular diseases
Cytokines - metabolism
Echocardiography
Endothelin 1
Endothelin-1 - blood
Endothelin-1 - genetics
Endothelin-1 - metabolism
Enzyme-Linked Immunosorbent Assay
Gene expression
Heart
Heart - physiopathology
Humanities and Social Sciences
Hypertrophy
Light microscopy
Male
Mandible
Microscopy
mRNA
multidisciplinary
Myocardium
Myocardium - metabolism
Myocardium - pathology
Occlusal Splints
Palate
Polyacrylamide
Polymerase chain reaction
Polysomnography
Rabbits
RNA, Messenger - metabolism
Science
Science (multidisciplinary)
Sleep
Sleep apnea
Sleep Apnea, Obstructive - chemically induced
Sleep Apnea, Obstructive - therapy
Sleep disorders
Structure-function relationships
Transmission electron microscopy
Ventricle
Ventricular Dysfunction, Left - pathology
title Mandibular Advancement Devices Prevent the Adverse Cardiac Effects of Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS)
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