高壓氧專家-範美高氧生醫科技股份有限公司

2017,10月

深耕美國加拿大市場15年，響譽國際高壓氧市場，如今深獲國際市場的肯定。菲律賓政府直接來台下訂單採購範美公司所生產之高壓氧醫療艙單人與多人艙。 more

2017,10月

缺氧易衰老？淺談高壓氧許多民眾甚至醫師，都因為百年前的翻譯誤差，以為氧氣會增加過氧化物，導致細胞衰老，Oxidation翻譯為氧化，是指失去一個電子的過程，而Oxygenation實際上應該被翻譯為「氧合」，意思是與氧氣結合。氧化過渡／過氧化是目前普遍認為細胞老化與死亡的原因，而氧合則與氧化毫不相關，這我們在談到氧氣與衰老前首先要有的第一觀念。 __________________________________________________________________ ✔ 什麼是高壓氧治療？高壓氧治療（Hyperbaric Oxygen Therapy，HBOT）是將病人置於大於一大氣壓的高壓艙內，給予100%的氧氣使病患吸入的一種治療方式。只在一大氣壓下呼吸純氧，或以不純的氧氣做體外治療的話，皆不列為高壓氧治療。 ✔ 高壓氧治療有哪些作用？〈1〉提高對厭氧性細菌的抵抗力，對於氣壞疽、厭氧性細菌感染、壞死性軟組織感染有一定療效。〈2〉提高白血球吞噬能力。〈3〉活化已經在血液循環之中的毒素，同時可以抑制病原體毒素分泌產生。〈4〉加速傷口癒合，提高纖維母細胞增生，製造膠原蛋白、造骨細胞，形成骨髓，可治療骨髓炎、放射線骨壞死及難癒合之骨折。〈5〉促使血管收縮，血管收縮後使血流減少，可減少組織水腫；且組織含氧量因高壓氧可提高10～15倍，所以組織亦不會缺氧。〈6〉血管新生作用，動物研究及臨床觀察卻有實效。高壓高濃度的氧氣可以刺激新生血管，加速一氧化碳和血色素分離，以及血管內氣泡分解，具有很強的穿透力，不依賴線粒體供能，可直接注入細胞核內，使氧能夠行使其職責。當線粒體有毛病時，常壓氧不能被線粒體利用，又不能穿入細胞核內，就會在細胞外和細胞漿內大量堆積而形成氧自由基，結果會使細胞凋亡。因此缺血時如果輸入常壓氧會加重細胞凋亡，而用高壓氧則可抑制細胞凋亡。 ✔ 高壓氧可用於治療哪些病症？氧氣在血中濃度提高，會使血管收縮、血流量減少約1/5，因此可以用於治療腦水腫、脊椎神經受傷、燙傷以及腔室症候群，而高壓氧本身則可以減小組織及循環中氣泡的體積，可治療體栓塞症和減壓症。受傷部位血流量減少的同時，組織的含氧量則會因為高壓氧治療反而增加，細胞內的氧分壓也會增高，達到活化細胞的作用，對許多功能性疾病有極佳的治療效果。因為週邊循環不良而缺氧，是許多慢性功能性疾病發生的原因，如關節炎、肌膜疼痛、麻木、暈眩、皮膚腫脹、肝功能不全、腎功能不良、心肌缺氧等，許多疾病都是如此。善加利用高壓氧可以有極佳的治療與預防。慢性疲勞症候群與性別、種族、氣候、體質、工作性質、壓力、生活習慣等因素息息相關，但都會對身體功能產生極大影響。現代人也常有身體疲倦及睡眠不足等狀況，主要是因為全身各個微小週邊循環與組織，慢性長期缺氧累積氧債與低濃度毒素，以及新陳代謝中的酸累積、毒素排除過慢，使人感到疲勞與身體功能不良。高壓氧治療可以使新陳代謝完全，毒素累積減少並加速排除，對各細胞、組織與器官的功能都有極大幫助，而降低慢性疲勞症候群的嚴重性與發生率。此外，高壓氧治療對於運動傷害也有極佳治療與預防效果。運動傷害的成因分為急性與慢性，急性運動傷害如扭傷肌腱炎等，大多伴隨著神經與微血管傷害，還會因為水腫與缺氧而加重二度傷害；慢性運動傷害與疾病也多是因為修復期間的不當修養與治療而造成。接受高壓氧治療後，還能提升運動員的訓練成績。 ✔ 高壓氧是否能達到美容的效果？目前對於高壓氧治療，美容專家有三種說法：一種說有美容抗老作用，一種說沒有美容抗老作用，第三種還說有「醜容促老」作用。理由是高壓氧只是增加體內氧濃度，促進體內氧化，使氧自由基增加、細胞凋亡産生催老作用。其實肌膚與一般細胞的老化原因有許多，細胞內的含氧量減少是其中重要的一點，經常使用高壓氧可以降低氧債與毒素累積並活化免疫力，使身體長保健康與年輕。臨床經驗告訴我們：手指末節離斷只經簡單縫合（因末梢血管太細不能縫合）後，可以通過高壓氧治療成功，而高壓氧對長期不癒的骨折、臨床上一大難題的糖尿病足也有十分好的療效，可得出高壓氧對組織生長有十分好的促進作用。而生長與凋亡是一個平衡體系，因此高壓氧對細胞凋亡應該有一定的抑制作用，而不會造成所謂的「醜容促老」後果。蔡啟聖醫師學經歷：凱薾抗衰老醫學中心院長｜台灣抗衰老再生醫學會理事長｜聖路易大學公衛博士｜聖路易大學醫管碩士｜國防醫學院學士｜中山醫學大學學士｜中山醫學大學傑出校友｜國泰醫學中心醫師｜龍潭敏盛醫院院長｜範美高氧生醫科技(股)公司董事長專長：神經外科專科醫師｜一般外科專科醫師｜抗衰老再生醫學｜高壓氧專科醫師｜幹細胞研究｜老人醫學｜功能醫學 more

2017,10月

輕高壓氧

Journal of Scientific Research & Reports 3(14): 1886-1896, 2014; Article no. JSRR.2014.14.005 SCIENCEDOMAIN international www.sciencedomain.org 科學究與報告雜誌 3(14): 1886-1896 ，2014; 文章號碼。 JSRR.2014.14.005 SCIENCEDOMAIN 科學構成 Exposure to Mild Hyperbaric Oxygen Increases Blood Flow and Resting Energy Expenditure but not Oxidative Stress 輕度高壓氧增加血流量和靜息時能量消耗但不增加氧化壓力 Akihiko Ishihara1*, Fumiko Nagatomo1, Hidemi Fujino2 and Hiroyo Kondo3 秋彥石原慎太郎1 * 經史子集永友1 秀美藤野2 和博譽近藤3 1Laboratory of Cell Biology and Life Science, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto 606-8501, Japan. 2Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Kobe 654-0142, Japan. 3Department of Food Sciences and Nutrition, Nagoya Women’s University, Nagoya 467-8610, Japan. 1 細胞生物學和生命科學，可以究生院的人類和環境實驗室可以究中、京都大學京都 606 8501 ，日本。 2 康復科科學、健康科學、神戶大學可以究生院科比 654-0142 ，日本。 3 部的食品科學與營養、名古屋女子大學、名古屋 467-8610 ，日本。 Authors’ contributions This work was carried out in collaboration between all authors. All authors read and approved the final manuscript. 這項工作是在所有的作者之間的協作進行的。所有作者都閱讀和通過最後的手稿。 Received 14th March 2014 Accepted 29th May 2014 Published 16th June 2014 14th2014 年 3 月收到29th2014 年 5 月接受16th2014 年 6 月出版 ABSTRACT *Corresponding author: E-mail: [email protected]; 摘要目的︰本研究探討輕度高壓氧暴露對血流量和靜息能量消耗的影響。研究設計︰臨床研究。方法︰ 14 個健康婦女接受溫和高壓氧條件在 1.25 大氣絕對 36.0%氧為 50 分鐘。他們心率、週邊血氧飽和度、血流量、靜息能量消耗，產生活性氧代謝及潛在的生物抗氧化劑進行監測，並以治療前後值進行比較。結果︰心率下降溫和高壓氧暴露後。相反，週邊血氧飽和度、血流量和靜息能量消耗於治療後增加。活性氧代謝物或生物抗氧化劑的水準沒有變動。結論︰溫和高壓氧暴露增加血流量和代謝而不會增加氧化壓力。 Keywords: Biological antioxidant potential; blood flow; derived-reactive oxygen metabolites; heart rate; mild hyperbaric oxygen; peripheral oxygen saturation; resting energy expenditure. 關鍵字︰生物抗氧化劑潛力; 血流量; 匯出了活性氧代謝產物; 心率; 溫和的高壓氧; 週邊的血氧飽和度; 靜息能量消耗。 1. INTRODUCTION簡介 An elevation in atmospheric pressure accompanied by an increase in oxygen concentration enhances the partial pressure of oxygen and increases the levels of oxygen dissolved in plasma. Hyperbaric conditions at 2–3 atmospheres absolute (ATAs) with an oxygen concentration of 100% are generally used for hyperbaric oxygen therapy [1,2]. Hyperbaric oxygen therapy is used for the treatment of temporary hypoxia [3], tissue repair after burn injury [4], intractable ulcer [5,6], open fractures, and crush injuries [7]. However, the conditions used in hyperbaric oxygen therapy are thought to induce the excessive production of reactive oxygen species in several tissues and organs [8]. 海拔在大氣壓力伴隨中氧濃度的增加提高氧分壓、增加血漿中的溶解氧水準。 2 — 3 絕對大氣壓下 (ATAs) 100%氧氣濃度高壓氧條件通常用於高壓氧治療 [1，2]。高壓氧治療用於臨時缺氧 [3] [4]、燒傷後組織修復治療難治性潰瘍 [5，6]、開放性骨折、壓碎傷 [7]。在高壓氧治療使用的條件被認為是促使過度生產的幾個組織中的活性器官氧物種、 [8]。 In previous studies, we found that mild hyperbaric conditions (1.25 ATAs with 36.0% oxygen) can be used to increase oxidative capacity in cells and tissues [9,10]. Whereas concentrations of oxygen higher than 40% cause side effects such as enhanced levels of oxidative stress [11] and/or increased numbers of invasive inflammatory cells [12], conditions of mild hyperbaric oxygen do not cause enhanced levels of oxidative stress [11]. In addition, we previously observed in animal experiments that type 2 diabetes [13–16], diabetes- induced cataracts [17], hypertension [18], type II collagen-induced arthritis [19], and age- related decline in muscle oxidative enzyme activity [20] were inhibited and/or improved by exposure to mild hyperbaric oxygen. 我們發現高壓氧條件溫和(36.0%氧氣體 1.25 ATAs)可以增加細胞和組織氧化能力[9，10]。而高於 40%的氧濃度導致副作用、例如增強的氧化應激 [11] 級別和/或增加發炎性細胞數目 [12]、輕度高壓氧條件不會導致氧化應激 [11] 增強的水準。此外，我們以前發現第 2型糖尿病 [13-16]、致糖尿病白內障 [17] [18]，高血壓的動物實驗中觀察到第二型 II 膠原誘發的關節炎 [19]、和與年齡有關的肌肉氧化的酶活性 [20] 可以因溫和高壓氧治療而使之下降抑制和/或改進。 We estimate that the amount of oxygen dissolved in plasma under mild hyperbaric conditions is 2.76 times greater than that under normal conditions, when the atmospheric pressure is 1.25 times greater and the oxygen concentration is 1.72 times higher than normal. Thus, it is plausible that the increased dissolved oxygen enhances metabolism in cells and tissues. In this study, we examined the effects of exposure to mild hyperbaric oxygen on blood flow and resting energy expenditure. Healthy women were exposed to mild hyperbaric conditions for 50 min. Values for heart rate, peripheral oxygen saturation (SpO2), blood flow, resting energy expenditure, derived-reactive oxygen metabolites (dROMs), and biological antioxidant potential (BAP) were obtained before and after exposure to mild hyperbaric oxygen and then compared. dROMs and BAP were used as indices of oxidative stress and antioxidant capacity, respectively. Our results show that exposure to mild hyperbaric oxygen increases blood flow and metabolism without increasing levels of oxidative stress. 我們估計、在溫和的高壓氧條件下血漿中溶解的氧氣量2.76倍、正常條件下、當大氣壓力是1.25倍和氧濃度比正常高出1.72倍。因此，這是合理增加溶解的氧增強代謝的細胞和組織。在此可以究中，我們審查了輕度高壓氧暴露對血流量和靜息能量消耗的影響。健康婦女被暴露溫和高壓氧條件為 50 分鐘：心率、週邊血氧飽和度值 (SpO2)、血流量增加、靜息能量消耗，產生活性氧代謝產物 (dROMs) 和生物抗氧化劑潛在 (BAP) 治療前前和溫和型高壓氧治療後、進行比較。分別以 dROMs 和 BAP 為氧化應激和抗氧化能力的指標。我們的結果顯示，輕度高壓氧氧治療增加血流量和代謝不增加的化水準應力。 2. MATERIALS AND METHODS 材料和方法 Participants and Exposure to Mild Hyperbaric Oxygen For this study, we used a mild hyperbaric oxygen chamber that we had designed for use in human experiments (Japan Patent No. 5076067, dated September 7, 2012). The chamber consists of an oxygen tank (length, 240 cm; width, 95 cm; height, 95 cm; weight, 140 kg) in which a single participant could lie down and a control box (length, 55 cm; width, 50 cm; height, 120 cm; weight 70 kg) containing an oxygen concentrator and an air compressor. The atmospheric pressure and oxygen concentration were controlled using a computer -assisted system in the control box. The interior of the mild hyperbaric oxygen chamber was automatically maintained at a temperature of 22±2ºC with a relative humidity of 45–55%. Using this chamber, 14 healthy women (age, 18.4±0.5 years; height, 1.58±0.03 m; body weight, 48.9±3.3 kg; body mass index, 19.5±0.9 kg·m-2; values are means ± standard deviations) were first exposed to normobaric conditions (1.00 ATA with 20.9% oxygen) for 50 min as the control. The same participants were then exposed to mild hyperbaric oxygen for 50 min on a subsequent day. 這項究中、我們使用溫和高壓氧艙內、我們設計了用於人體實驗 (日本專利號 5076067、 2012 年 9 月7日)。分別由各組的每個參與者躺入氧氣罐 (長度、 240 釐米; 寬度、95釐米高度，95釐米; 重140公斤) 和一個控制盒 (長度、 55 釐米寬，50 釐米; 高度，120釐米; 重70公斤) 含製氧機和空氣壓縮機。電腦控制大氣壓力和氧氣濃度在控制項框中的輔助的系統。內部，溫和高壓氧艙內自動維持每 22±2ºC 溫度與相對濕度為 %45-55%。使用這個溫和高壓氧艙，實驗者為一組14名健康婦女 (年齡18.4±0.5 歲; 高度1.58±0.03 米; 體重 48.9±3.3公斤; 體重指數，19.5±0.9 kg·m-2; 值 ± 標準差) 控制組：常壓條件 (20.9%氧氣體 1.00 ATA) 每一次治療為 50分鐘。相同一組的參與者，在第二天，治療條件為：在 1.25 絕對大氣壓、氧濃度36.0% 共 50 分鐘溫和高壓氧治療。 2.2 Heart Rate and SpO2 Heart rate (beats/min) and SpO2 (%) were monitored on the right forefinger of each participant, with the participant in a supine position, using a pulse oximeter (PULSOX–300i; Konica–Minolta Sensing Co., Ltd.; Sakai, Japan) before and after exposure to normobaric conditions or mild hyperbaric oxygen. 2.2 心率和 SpO2 心率 (次/分) 和 SpO2(%）參與者以仰臥位、使用右手指以脈搏血氧儀 ((PULSOX–300i; Konica–Minolta Sensing Co., Ltd.; Sakai, Japan)量測；常壓條件與溫和型高壓氧治療前後。 2.3 Blood Flow Blood flow (mL/min/100 g tissue) was measured using a laser Doppler flowmeter (FLO–N1; NeuroScience, Inc.; Tokyo, Japan). The flowmetry probe was attached to the back of the participant’s right hand. Blood flow was continuously measured during exposure to normobaric conditions or mild hyperbaric oxygen. The data were transferred to a personal computer via an interface (EFA/400; Distributed Design Concept; Dover, NH, USA) from the flowmeter and analyzed using the data recording software LogWorx, ver. 1.804 (Distributed Design Concept). 2.3 血流使用鐳射多普勒血流儀; (FLO–N1; NeuroScience, Inc.; Tokyo, Japan)測定血流量 100 g ，（毫升，min組織)短片）。血流儀探頭被附加到參與者的右手背。在常壓條件或溫和高壓氧治療期間連續測定血流量。資料傳輸到個人電腦通過介面 (EFA/400;分散式的設計理念;多佛，新罕布希爾州，美國) 從流量計和分析使用資料記錄軟體 LogWorx 版 1.804 (分散式設計概稔)。 2.4 Resting Energy Expenditure Resting energy expenditure (kcal) was measured using a metabolic analyzer (MedGem indirect calorimeter; Microfile, Medical Home Solutions, Inc.; CO, USA) before and after exposure to normobaric conditions or mild hyperbaric oxygen. The data were transferred to a personal computer and analyzed using the software MedGem Analyzer (Microfile, Medical Home Solutions, Inc.). 2.4 靜息能量消耗靜息能量消耗（千卡）測定了代謝分析儀（MedGem 間接量熱儀;Microfile、醫學家用解決方案公司; CO、美國) 在常壓條件或輕度高壓氧治療前後。資料傳輸到個人電腦，並分析了使用軟體 MedGem 分析儀 (Microfile，醫學家用解決方案，Inc.)。 2.5 dROMs and BAP The levels of dROMs and BAP were estimated before and after exposure to normobaric conditions or mild hyperbaric oxygen. Blood samples were obtained from the left forefinger. A free radical and antioxidant potential determination device (Free Radical Analytical System 4; Health & Diagnostics; Grosseto, Italy) was used to measure the levels of dROMs and BAP [21,22]. dROM values indicate serum hydroperoxide levels and are obtained by measuring the amount of N, N-diethyl-p-phenylenediamine oxidized by hydroperoxide-derived free radicals from the plasma sample [23, 24]. dROMs are expressed in Carr unit, named after an Italian biologist who designed a scale based on data from >5000 nonsmoking, healthy participants aged 14–80 years (1 Carr unit = 0.08 mg hydroperoxide/100 mL H2O2) [21]. The average level of dROMs for healthy individuals is approximately 300 Carr units [23]. BAP levels are determined based on the capacity of the plasma sample to reduce ferric ions to ferrous ions [24]. 2.5 dROMs 和BAP DROMs和BAP的含量估計之前和之後暴露在常壓條件下或溫和型高壓氧。血液樣品從左食指。自由基和抗氧化電位測定裝置 (自由基分析系統 4;健康與診斷;佛羅倫斯，義大利) 用來測量水準的 dROMs 和 BAP [21，22]。 dROM 值表明血清過氧化氫和測定 N，N-二乙基-p-苯二胺氧化氫過氧化物自由基從血漿樣品 [23，24] 大量獲得。 dROMs 表示在卡爾單元中、義大利的生物學家、他設計了一個基於資料從刻度的名字命名 > 5000 不吸煙、健康參與者年齡在 14 — 80 歲 (1 卡爾單位 = 0.08 毫克過氧化氫100 毫升 H2O2) [21]。 DROMs 健康的人的平均水準是大約卡爾單位 300 [23]。基於血漿樣品減少鐵離子和亞鐵離子的能力來確定 BAP 水準 [24] 2.6 Statistical Analysis Means and standard deviations were calculated from individual values using standard procedures. The Student’s t–test was used for statistical comparisons; significance was indicated by a P-value <0.05. 2.6 統計分析。從使用標準程式的單個值，計算均值和標準差。學生t-測試用於統計的比較;意義表示由 P -值< 0.05。 3. RESULTS Heart Rate There was no change in heart rate after exposure to normobaric conditions (Fig. 1A). In contrast, the heart rate decreased after exposure to mild hyperbaric oxygen (Fig. 1B). SpO2 There was no change in SpO2 after exposure to normobaric conditions (Fig. 1C). In contrast, the SpO2 increased after exposure to mild hyperbaric oxygen (Fig. 1D). Fig. 1. Heart rate (A and B) and peripheral oxygen saturation (C and D) under normobaric (A and C) and mild hyperbaric (B and D) conditions Values are means and standard deviations obtained from 14 participants; *P < 0.05 3. 結果 3.1 心律暴露在常壓條件下 (圖 1A)後心率無變化。相比之下，心率溫和型高壓氧 (圖 1B) 治療後有所下降。 3.2 SpO 2 暴露在常壓條件下SpO2沒有變化後(圖 1)。相比之下，溫和型高壓氧治療後SpO2增加(圖 1)。圖 1 。心率 (A 和 B) 和周邊氧飽和度 (C 和 D) 在常壓 (A 和 C) 和溫和的高壓氧 (B 和 D) 條件下值的均值和標準差從 14 參與者; 有關人等* P < 0.05 3.3 Blood Flow Fig. 2 shows the blood flow of a participant under normobaric (top trace) and mild hyperbaric (bottom trace) conditions for 50 min. There was no change in blood flow after exposure to normobaric conditions (Fig. 3A). In contrast, the blood flow effectively doubled (from 2.7±0.5 mL/min/100 g tissue to 5.3±0.8 mL/min/100 g tissue) after exposure to mild hyperbaric oxygen (Fig. 3B). 3.3 血流圖2顯示參與者寫留在常壓（頂級跟蹤）和溫和型高壓氧下（井底軌跡）如下︰為 50 分鐘。常壓條件 (圖 3A) 暴露後沒有任何變化，而溫和型高壓氧治療後，血液流動有效地增加了一倍 (從 2.7±0.5 到 5.3±0.8 毫升，分鐘，100 g 組織毫升，分鐘，100 g 組織) 後暴露于輕度高壓 (氧圖 3B)。圖 2 。血流量的常壓（頂部）和輕度高壓氧下代表參與者（底部）如下︰ 50 分鐘 Fig. 2. Blood flow of a representative participant under normobaric (top) and mild hyperbaric (bottom) conditions for 50 min Resting Energy Expenditure There was no change in resting energy expenditure after exposure to normobaric conditions (Fig. 3C). In contrast, the resting energy expenditure increased by 10.2% (from 1181±125 kcal to 1296±121 kcal) after exposure to mild hyperbaric oxygen (Fig. 3D). Fig. 3. Blood flow (A and B) and resting energy expenditure (C and D) under normobaric (A and C) and mild hyperbaric (B and D) conditions Values are means and standard deviations obtained from 14 participants; *P < 0.05 圖 3 。血流量 (A 和 B) 和靜息能量消耗 (C 和 D) 在常壓 (A 和 C) 和溫和的高壓氧 (B 和 D) 條件下值的均值和標準差從 14 參與者; 有關人等* P < 0.05 3.4 靜息能量消耗在常壓條件下實驗，並沒有任何變化在靜息能量消耗(圖 3)。相比之下，JP CK6VU/6高壓氧 (圖 3D) 54XUL6後，增加了 10.2%(從到 1181±125 1296±121 千卡千卡) 靜息能量消耗。 3.5 dROMs and BAP There was no change in the level of dROMs or BAP after either exposure to normobaric conditions or mild hyperbaric oxygen (Fig. 4). Fig. 4. Derived-Reactive oxygen metabolites (dROMs; A and B) and biological antioxidant potential (BAP; C and D) under normobaric (A and C) and mild hyperbaric (B and D) conditions Values are means and standard deviations obtained from 14 participants 圖 4 。匯出了活性代謝氧產物 (dROMs; 和 B) 和生物抗氧化劑潛在 (BAP;C 和 D) 在常壓 (A 和 C) 和溫和的高壓氧 (B 和 D) 條件下值的均值和標準差從 14 參與者獲得 3.5 dROMs 和BAP 暴露在常壓條件下或輕度高壓氧後的dROMs或BAP程度沒有變化(圖 4)。 4. DISCUSSION Hyperbaric oxygen therapy leads to vasoconstriction and hyperoxygenation, making it an effective treatment option for patients with various clinical disorders such as severe carbon monoxide poisoning, decompression sickness, and arterial gas embolism, and as adjunctive therapy for the prevention and treatment of osteoradionecrosis, clostridial myonecrosis, and compromised skin grafts and flaps [1,2]. During hyperbaric oxygen therapy, patients are generally exposed to 2–3 ATAs with 100% oxygen. However, a previous study [25] reported that exposure to hyperbaric conditions (2.5 ATAs with 100% oxygen for 2–2.5 h, 3 times per week, up to 100 times) induced cataracts in 17- to 18-month-old guinea pigs. Similarly, myopia and cataracts developed in human lenses after exposure to prolonged hyperbaric conditions at 2–2.5 ATAs with 100% oxygen for 1.5 h, once per day, from 150 to 850 times [26], although rarely after only 48 times [27]. Therefore, exposure to hyperbaric conditions at 2–3 ATAs with 100% oxygen has the potential to induce and accelerate myopia and cataracts. In addition, standard hyperbaric oxygen therapy is thought to cause excessive production of reactive oxygen species in several tissues and organs [8,28], suggesting that oxidative stress induced by hyperbaric oxygen therapy may accelerate tissue damage. Oxidative stress occurs when the production of oxidants exceeds the capacity to neutralize them, and oxidative stress levels resulting from exposure to hyperbaric conditions depend not only on pressure but also on the duration of the exposure; a pressure of exposure of 2.5–3 ATAs and a duration of exposure of 90–120 min result in a pronounced increase in the level of oxidative stress [29,30]. We determined that exposure to mild hyperbaric conditions at 1.25 ATAs with 36.0% oxygen is sufficient to obtain effective responses in oxidative capacity in cells and tissues [9,10]. However, there are no data available concerning the response of oxidative stress and/or the levels of reactive oxygen species in patients exposed to mild hyperbaric oxygen. Therefore, in this study, we examined dROMs as an index to ascertain the level of oxidative stress in healthy humans exposed to mild hyperbaric oxygen. We found that there were no changes in the dROMs after exposure to mild hyperbaric oxygen (Fig. 4B). Interestingly, our previous study [19] showed that exposure to mild hyperbaric oxygen was effective at reducing levels of oxidative stress and C-reactive protein, which were pronounced as the result of type II collagen-induced arthritis in rats. Similarly, high blood pressure and enhanced levels of oxidative stress in spontaneously hypertensive rats were reduced by exposure to mild hyperbaric oxygen [18]. Increased sympathetic activation in hypertensive rats is mediated by the overproduction of toxic reactive oxygen species [31]. Therefore, a reduction in oxidative stress may underlie the decrease in high blood pressure observed in hypertensive rats exposed to mild hyperbaric oxygen. The results of this study using human participants, combined with the previous findings using experimental animals [18, 19], lead to the conclusion that exposure to mild hyperbaric oxygen does not affect levels of oxidative stress. Our previous studies [9,10,13–20] using experimental animals demonstrate that exposure to mild hyperbaric oxygen increases and improves metabolism in cells and tissues. In one study [10], developing rats exposed to mild hyperbaric oxygen exhibited greater voluntary running activities compared with animals maintained under normobaric conditions, and the oxidative enzyme activities in fibers of the soleus and plantaris muscles and in motoneurons of the spinal cord that innervate these skeletal muscles increased after exposure to mild hyperbaric oxygen. Another study [20] found that an age-related decrease in oxidative capacity of skeletal muscles (e.g., a decreased percentage of high-oxidative fibers and reduced oxidative enzyme activity in the tibialis anterior muscles) of mice was reversed by exposure to mild hyperbaric oxygen. Interestingly, the skeletal muscles of Goto–Kakizaki rats with nonobese type 2 diabetes have a low oxidative capacity compared with those of nondiabetic rats [32]. In addition, the skeletal muscles of obese Long–Evans Otsuka Tokushima fatty and Zucker diabetic fatty rats, which are both type 2 diabetes animal models, contain a lower percentage of high-oxidative fibers [33,34]. These findings suggest that the low oxidative capacity of skeletal muscles in rats with type 2 diabetes may be associated with insulin resistance and impaired glucose metabolism. The growth-associated increase in blood glucose levels in rats with type 2 diabetes was attenuated by exposure to mild hyperbaric oxygen [13–15]. Furthermore, exposure to mild hyperbaric oxygen reduced high blood glucose levels and improved oxidative capacity in the skeletal muscles of adult rats with type 2 diabetes, and these effects were maintained under subsequent normobaric conditions [16]. In this study, the amount of dissolved oxygen was estimated to have increased by 2.76 times (0.864 mL/dL after exposure to mild hyperbaric oxygen/0.313 mL/dL under normobaric conditions) after exposure to mild hyperbaric oxygen. The amount of dissolved oxygen was estimated as follows: under normobaric conditions (1.00 ATA and 20.9% oxygen), the partial pressure of oxygen in the alveolus = (760  47) × 0.209 – 40 / 0.8 + (40 × 0.209) × (1 – 0.8) / 0.8 = 101.11 mmHg; therefore, the amount of dissolved oxygen under normobaric conditions is 0.0031 mL/dL/mmHg × 101.11 mmHg = 0.313 mL/dL. In contrast, under mild hyperbaric conditions, the partial pressure of oxygen in the alveolus = (950 – 47) × 0.360 – 40 / 0.8 + (40 × 0.360) × (1 – 0.8) / 0.8 = 278.68 mmHg; therefore, the amount of dissolved oxygen under mild hyperbaric conditions is 0.0031 mL/dL/mmHg × 278.68 mmHg = 0.864 mL/dL, where 1.00 ATA = 760 mmHg, 1.25 ATAs = 950 mmHg, water vapor pressure = 47 mmHg, the concentration of carbon dioxide in the alveolus = 40 mmHg, and the respiratory exchange ratio = 0.8. This study showed that the blood flow in human participants effectively doubled after exposure to mild hyperbaric oxygen (Fig. 3B). It is widely known that endurance exercises cause a steady increase in blood flow. However, the increase in blood flow following an endurance exercise is induced mostly in active skeletal muscles but not in internal organs. In addition, because of the increased atmospheric pressure, exposure to mild hyperbaric oxygen has an advantage in that it can increase the amount of dissolved oxygen in plasma, which does not occur with endurance exercises. This study also found that the resting energy expenditure in participants increased by 10.2% after exposure to mild hyperbaric oxygen (Fig. 3D). 4. 討論高壓氧治療會導致血管收縮和氧使其成為各種臨床疾病如重度一氧化碳中毒、減壓病和動脈氣體栓塞症，以及輔助治療的預防和治療頜骨放射性骨壞死，魏氏梭菌後，患者的有效治療方法，皮瓣皮膚移植等 [1，2]。在高壓氧治療、患者一般暴露于 2 — 3 ATAs 與 100%的氧氣。先前的 [25] 研究：17 到 18 個月的幾內亞豬，暴露在高壓氧條件下 (2 —2.5 h 的 100%氧氣的 2.5 ATAs，每週三次，做100 次) 會誘導白內障生成。同樣，近視、白內障等疾病在人類長期暴露在高壓氧在 2 – 2.5 ATAs 用 100%氧氣的條件下為 1.5 h，每天一次，從 150 到 850 次 [26]，雖然很少發生，但也有只48 次便發生的報告 [27]。因此，暴露在高壓氧條件下，在 2 — 3 ATAs 與 100%的氧氣有可能誘導近視、白內障等。此外，標準高壓氧治療被認為造成過度生產活性氧物種於幾個組織和器官 [8,28]、這表明高壓氧療法誘導的氧化應激可能加速組織損傷。氧化應激發生時的氧化劑生產超過能力壓制他們、和因暴露在高壓環境下的氧化應激水準取決於不僅對壓力也對持續時間的曝光。 2.5-3 ATAs 暴露及暴露時間的 90-120 分鐘結果 [29,30] 氧化應激水準明顯增加的壓力。我們確定接觸到溫和高壓氧條件在1.25 ATAs 36.0%氧氣是不會增加細胞和組織的氧化能力 [9，10]。因沒有研究與有關的氧化應激反應和（或）物種患者輕度高壓的活性氧氧暴露水準。因此，在本究中，我們以 dROMs 為確定氧化應激的健康人類對溫和高壓氧暴露程度的指標。我們發現，在 dROMs 後暴露于輕度高壓 (氧圖 4B) 沒有變化。有趣的是，[19] 我們先前的研究、接觸到溫和高壓氧是有效地降低氧化應激和 C-反應蛋白、第二類型的結果二膠原誘導性關節炎水準。同樣，血壓高的壓力和自發性高血壓大鼠氧化應激增強的水準減少了暴露于溫和高壓氧 [18]。及高血壓大鼠增加的交感神經介導生產過剩的有毒活性氧物種 [31]。因此，在化應激可能減少基礎觀察輕度高壓氧氧暴露的高血壓大鼠血壓高的壓力減少。使用人類的參與者，結合前人的成果，使用實驗動物 [18，19]、本可以究的結果得出結論，暴露于溫和高壓氧不影響水準的氧化應力。我們以往的[9,10,13-20] 實驗動物展示、暴露于溫和高壓氧，提高了細胞和組織的代謝。在一項 [10]、發育期大鼠溫和高壓氧治療發展出更多自願運行活動，相對維持在常壓條件下的動物和氧化的酶活動的比目魚肌和蹠肌肉纖維並在脊髓運動神經元的支配這些骨骼肌肉輕度高壓氧暴露後增加。另一項 [20] 發現、由於溫和高壓氧治療，骨骼肌 (高氧化纖維和脛前肌減少氧化的酶活性的下降百分比) 的小鼠氧化能力與老化減少。有趣的是，非肥胖的 2 型糖尿病大鼠骨骼肌有低的氧化能力，相比那些非糖尿病大鼠 [32]。此外，肥胖長埃文斯大塚德島脂肪肝和 Zucker 糖尿病脂肪肝大鼠、這兩者都是骨骼肌鍵入 2 糖尿病動物模型，包含高氧化纖維 [33,34] 的比例較低。這些結果表明，低氧化能力的類型 2 型糖尿病可能與大鼠骨骼肌是與胰島素抵抗及糖代謝異常相關聯。型糖尿病大鼠血糖水準的生長相關增加瘦了暴露于輕度高壓氧 2 [13-15]。此外，溫和高壓氧暴露降低高血糖水準和改進氧化能力的成人 2 型糖尿病大鼠骨骼肌和這些影響被維持在隨後常壓條件下 [16]。 5. PERSPECTIVES AND OPERATIVE APPLICATIONS We previously observed in animal experiments that lifestyle-related diseases (e.g., type 2 diabetes [13–16], diabetes-induced cataract [17], and hypertension [18]) were inhibited and/or improved by exposure to mild hyperbaric oxygen. Based on the previous findings from animal models [13–18] and our observations of increased blood flow and resting energy expenditure in participants in this study, we suggest that exposure to mild hyperbaric oxygen may be an effective therapy for patients with type 2 diabetes and/or hypertension. In the future, we intend to study the effects of exposure to mild hyperbaric oxygen on disrupted nervous functions (e.g., autonomic ataxia, emotional instability, and/or dementia). 5 。前瞻觀點和實際適應我們以前在動物實驗中觀察到、與生活方式有關的疾病 (如 2 型糖尿病 [13-16]、誘導糖尿病白內障 [17] 和 [18] 高血壓)，可因溫和高壓氧治療而得到抑制或改進。基於前人的成果，從動物模型 [13-18] 和我們的血流量增加和靜息能量消耗的研究、我們建議、溫和高壓氧可能是 2 型糖尿病和（或）高血壓患者治療的有效方法。今後，我們打算以研究溫和高壓氧治療對已破壞的神經功能的影響 (例如自主神經失調、情緒不穩定，和老年癡呆。 6. CONCLUSION We conclude that exposure to mild hyperbaric oxygen increases blood flow and metabolism without increasing levels of oxidative stress. 6. 結論我們得出結論、暴露于輕度高壓氧增加血流量和代謝而不會增加氧化應激水準。 CONSENT Participation in the study was voluntary. Each participant received an explanation as to the aims of the study and methods of data collection and signed an informed consent form. 意願參與這項可以究是自願的。每個參與者收到目標的可以究和資料收集的方法解釋、並簽署知情同意書。 ETHICAL APPROVAL All authors declare that all experiments have been examined and approved by the Institutional Experiment Committee of Kyoto University (Kyoto, Japan) and have been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki. 倫理委員會批准所有作者都聲明、所有的實驗都有了由審查和批准機構實驗委員會的京都大學（日本京都）並根據 1964年年的赫爾辛基宣言》所規定的道德標準進行了。 COMPETING INTERESTS This paper has not been presented previously in any form. No conflicts of interest have been reported by the authors or by any individuals in control of the content of this paper. 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Exp Eye Res. 1995;60:219–35. Palmquist BM, Philipson B, Barr PO. Nuclear cataract and myopia during hyperbaric oxygen therapy. Br J Ophthalmol. 1984;68:113–7. Gesell LB, Trott A. De novo cataract development following a standard course of hyperbaric oxygen therapy. Undersea Hyperb Med. 2007;34:389–92. Padgaonkar VA, Leverenz VR, Fowler KE, Reddy VN, Giblin FJ. The effects of hyperbaric oxygen on the crystallins of cultured rabbit lenses: a possible catalytic role for copper. Exp Eye Res. 2007;71:371–83. Oter S, Korkmaz A, Topal T, Ozcan O, Sadir S, Ozler M, et al. Correlation between hyperbaric oxygen exposure pressures and oxidative parameters in rat lung, brain, and erythrocytes. Clin Biochem. 2005;38:706–11. Öter S, Topal T, Sadir S, Özler M, Uysal B, Ay H, et al. Oxidative stress levels in rats following exposure to oxygen at 3 atm for 0–120 min. Aviat Space Environ Med. 2007;78:1108–13. Kishi T, Hirooka Y, Kimura Y, Ito K, Shimokawa H, Takeshita A. Increased reactive oxygen species in rostral ventrolateral medulla contribute to neural mechanisms of hypertension in stroke-prone spontaneously hypertensive rats. Circulation. 2004;109:2357–62. Yasuda K, Nishikawa W, Iwanaka N, Nakamura E, Seino Y, Tsuda K, et al. Abnormality in fibre type distribution of soleus and plantaris muscles in non-obese diabetic Goto–Kakizaki rats. Clin Exp Pharmacol Physiol. 2002;29:1001–8. Yasuda K, Ishihara A, Adachi T, Shihara N, Seino Y, Tsuda K. Growth-related changes in skeletal muscle fiber type and insulin resistance in diabetic Otsuka Long– Evans Tokushima fatty rats. Acta Histochem Cytochem. 2001;34:371–82. Adachi T, Kikuchi N, Yasuda K, Anahara R, Gu N, Matsunaga T, et al. Fibre type distribution and gene expression levels of both succinate dehydrogenase and peroxisome proliferator-activated receptor-g coactivator-1a of fibres in the soleus muscle of Zucker diabetic fatty rats. Exp Physiol. 2007;92:449–55. _ _ _ © 2014 Ishihara et al.; This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. more

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