nvestigating the Pathophysiology of Sleep Apnea from Nasal Nitric Oxide Production

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K18298
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 56050:Otorhinolaryngology-related
• Research Institution: Kansai Medical University
• Principal Investigator: KAWACHI Risaki 関西医科大学, 医学部, 助教 (70620756)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 呼気一酸化窒素 / 鼻腔FENO / 睡眠時無呼吸症 / OSA

Outline of Final Research Achievements

Nasal NO and nasal mucosa scraping fluid were compared before and after the introduction of CPAP in patients with severe OSA. Nasal NO decreased significantly after the introduction of CPAP. Induction of iNOS expression and NO production in the airway mucosa were considered relevant. In OSA, SIRT1 expression was decreased by hypoxic stress, HIF-1α expression was increased, and MIF and iNOS were induced. After transduction, SIRT1 expression was increased, HIF-1α was suppressed, and MIF and iNOS were inhibited. The changes were assumed to be due to the release of oxidative stress.

Free Research Field

睡眠時無呼吸症

Academic Significance and Societal Importance of the Research Achievements

OSAは近年ますます増加傾向にある疾患である。病勢の把握にはPSGが必要であるが決して簡易な検査ではない。OSAでは、睡眠中に反復する上気道閉塞に起因する酸化ストレスや炎症性サイトカインの上昇が、気道粘膜においてiNOS発現の誘導、NO 産生の亢進を来たすと考えられた。また、低酸素ストレスでSIRT1発現が低下、HIF-1α発現が更新し、MIFやiNOS(誘導型NO合成酵素)が誘導されることもわかり、CPAP導入で正常化されると示唆された。OSAの粘膜局所での変化を評価することでその病態を詳細に把握することができ、今後の無呼吸治療で病勢や治療効果を判定する一つの方法となる可能性が示唆された。