青少年近视眼预防与控制技术研究的新进展

doi:10.3877/cma.j.issn.2095-2007.2022.03.009

传统预防与控制近视眼的方法主要包括光学矫正、角膜塑形镜、离焦眼镜及其他手段。但此类方法尚不理想。目前，有研究结果表明，户外活动和低浓度阿托品对预防近视眼的发生和控制具有积极作用；轴性近视眼的发展与巩膜向近视眼方向重塑性有关，但机制尚不明确；眼轴增长而致的真性近视眼具有不可恢复或逆转的特点。长期航天飞行后会表现为后极部眼球扁平化、眼轴变短及屈光状态呈现远视性位移，表明受力环境变化可以影响巩膜重塑。因此，笔者认为结合适当的锻炼方式可促使血液头向转移和增加头眼部组织静水压力梯度，影响局部巩膜重塑，从而使眼轴向变短的方向发展或延缓眼轴增长的趋势，可作为近视眼预防与控制的新思路。

关键词: 近视眼预防与控制, 巩膜重塑, 眼轴长度, 体位改变

The traditional methods for the control of myopia development are optical correction, orthokeratology lens, defocus glasses and other methods, however, these approaches are poor. At present, it has been demonstrated that outdoor activities and the application of low concentration atropine had a positive effect on preventing the occurrence of myopia and controlling the growth of myopia diopter. The occurrence and development of axial myopia was related to scleral remodeling toward myopic direction, but the mechanism remains unclear. In addition, true myopia caused by the axial growth was irreversible. After long-term spaceflight, astronauts had posterior eyeball flattening, axial shortening, and hyperopic displacement of refractive state, indicating that stress environment could cause sclera remodeling. Therefore, the combination of appropriate exercise to promote the transfer of blood head and increase the hydrostatic pressure gradient of the head and eye tissue might affect the local scleral remodeling and shorten the axial direction of the eye, or delay the trend of axial growth, which could provide a new idea for the prevention and control of myopia.

Key words: Prevention and control of myopia, Scleral remodeling, Ocular axial length, Position change

图1 不同体位时眼球壁主要承受重力作用部位的示意图　图A~图D分别示坐位、倒立位、平卧位及倒俯卧位时眼球壁主要承受重力部位的示意图

表1 不同药物控制近视眼的文献汇总

第一作者	药物	实验对象	实验结果	实验结论
Zhu等^[27]	1%阿托品	平均年龄9岁儿童	随访24个月、25~36个月及36~48个月，使用1%阿托品药物患者的平均近视眼进展分别为(－0.27±0.81)D/年、(－0.31±0.29)D/年及(－0.41±0.23)D/年，轴向长度平均增加分别为(0.11±0.13)mm/年、(0.14±0.09)mm/年及(0.19±0.13)mm/年	1%阿托品可有效地调节眼部肌肉痉挛，延缓近视眼发展
Dong等^[32]	0.025~2.5 ng/μl多巴胺	3周龄豚鼠	结膜下注射多巴胺第11 d，豚鼠失焦眼和离焦眼的屈光度分别为－4.06 D和－3.64 D；且对剥夺型近视的抑制作用呈剂量依赖性	结膜下注射多巴胺可抑制形觉剥夺诱导性近视眼的形成
Seltner等^[33]	血管活性肠肽	雏鸡	血管活性肠肽注射8 d，雏鸡屈光度为－6.00 D近视眼，与未注射药物组眼轴长度的平均差异为0.6 mm，且对控制近视眼的进展呈剂量依赖性减少	球内注射血管活性肠肽可以有效地减少形觉剥夺诱导性近视眼形成，但不能完全消除
尹靓瑶等^[34]	褪黑素	1周龄豚鼠	腹腔注射外源性褪黑素10 mg/kg形觉剥夺近视眼的屈光度、眼轴长度、视网膜诱导性一氧化氮合酶及褪黑素受体表达分别为(－4.30±0.59)D、(8.044±0.24)mm、0.3733±0.0427及0.3743±0.0447	外源性褪黑素可抑制甚至逆转形觉剥夺豚鼠的屈光改变
Yu等^[35]	视黄酸	2周龄豚鼠	短波光暴露的豚鼠近视眼屈光度为(2.06±1.69)D，外源性视黄酸补充白光后，短波光组屈光度可恢复至(2.06±1.69)D	近视眼的视黄酸含量升高，且外源性补充视黄酸后可促进轴性近视眼的发生
Singh等^[36,37]	7－甲基黄嘌呤	Wistar大鼠和小鼠	7－甲基黄嘌呤对大鼠口服90 d和180 d，250 mg/kg、500mg/kg及1000 mg/kg的7－甲基黄嘌均无死亡率和毒性迹象，未观察到器官大小变化、囊肿形成、液体潴留及晶体形成的变化	7－甲基黄嘌呤皆有效地延缓近视眼发展，且安全性良好

表1 不同药物控制近视眼的文献汇总

第一作者	药物	实验对象	实验结果	实验结论
Zhu等^[27]	1%阿托品	平均年龄9岁儿童	随访24个月、25~36个月及36~48个月，使用1%阿托品药物患者的平均近视眼进展分别为(－0.27±0.81)D/年、(－0.31±0.29)D/年及(－0.41±0.23)D/年，轴向长度平均增加分别为(0.11±0.13)mm/年、(0.14±0.09)mm/年及(0.19±0.13)mm/年	1%阿托品可有效地调节眼部肌肉痉挛，延缓近视眼发展
Dong等^[32]	0.025~2.5 ng/μl多巴胺	3周龄豚鼠	结膜下注射多巴胺第11 d，豚鼠失焦眼和离焦眼的屈光度分别为－4.06 D和－3.64 D；且对剥夺型近视的抑制作用呈剂量依赖性	结膜下注射多巴胺可抑制形觉剥夺诱导性近视眼的形成
Seltner等^[33]	血管活性肠肽	雏鸡	血管活性肠肽注射8 d，雏鸡屈光度为－6.00 D近视眼，与未注射药物组眼轴长度的平均差异为0.6 mm，且对控制近视眼的进展呈剂量依赖性减少	球内注射血管活性肠肽可以有效地减少形觉剥夺诱导性近视眼形成，但不能完全消除
尹靓瑶等^[34]	褪黑素	1周龄豚鼠	腹腔注射外源性褪黑素10 mg/kg形觉剥夺近视眼的屈光度、眼轴长度、视网膜诱导性一氧化氮合酶及褪黑素受体表达分别为(－4.30±0.59)D、(8.044±0.24)mm、0.3733±0.0427及0.3743±0.0447	外源性褪黑素可抑制甚至逆转形觉剥夺豚鼠的屈光改变
Yu等^[35]	视黄酸	2周龄豚鼠	短波光暴露的豚鼠近视眼屈光度为(2.06±1.69)D，外源性视黄酸补充白光后，短波光组屈光度可恢复至(2.06±1.69)D	近视眼的视黄酸含量升高，且外源性补充视黄酸后可促进轴性近视眼的发生
Singh等^[36,37]	7－甲基黄嘌呤	Wistar大鼠和小鼠	7－甲基黄嘌呤对大鼠口服90 d和180 d，250 mg/kg、500mg/kg及1000 mg/kg的7－甲基黄嘌均无死亡率和毒性迹象，未观察到器官大小变化、囊肿形成、液体潴留及晶体形成的变化	7－甲基黄嘌呤皆有效地延缓近视眼发展，且安全性良好

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