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Long-term biomechanical properties of rabbit cornea after photodynamic collagen crosslinking

机译:光动力胶原交联后兔角膜的长期生物力学性能

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Purpose: Photodynamic riboflavin/ultraviolet-A (UVA)-induced collagen cross-linking, which increases the biomechanical stiffness of the human cornea by about 300%, has been introduced recently as a possible treatment for progressive keratoconus. The present study was undertaken to evaluate the longterm biomechanical effects of this new cross-linking treatment as a necessary prerequisite to its clinical success.Methods: The corneas of the left eyes of nine male rabbits were cross-linked. The contralateral eyes served as controls. After removal of the central 7 mm of the epithelium, the corneas were treated with the photosensitizer riboflavin and UVA irradiation for 30 mins with an irradiance of 3 mW/cm2 using a 370-nm UVA double diode. Groups of three animals were killed immediately after treatment and at 3 and 8 months, respectively. Biomechanical stress-strain measurements were performed using a microcomputer-controlled bio-material tester on 4 x 10-mm corneal strips.Results: Corneal thickness in the treated rabbit cornea was 408 +- 20 mum. A constant and significant increase in ultimate stress (of 69.7-106.0%), Young's modulus of elasticity (of 78.4-87.4%) and a decrease in ultimate strain (of 0.57-78.4%) were found over a time period of up to 8 months after cross-linking treatment.Conclusions: Riboflavin/UVA-induced collagen cross-linking leads to a long-term increase in biomechanical rigidity which remains stable over time. These data support our previous longterm clinical observations and give hope that this new treatment will halt progressive keratoconus definitively.
机译:目的:最近已引入光动力学核黄素/紫外线-A(UVA)诱导的胶原交联,该交联将人角膜的生物力学刚度提高了约300%,作为进行性圆锥角膜的一种可能治疗方法。本研究旨在评估这种新的交联疗法的长期生物力学效果,作为其临床成功的必要前提。方法:将9只雄性兔子的左眼角膜交联。对侧眼作为对照。除去上皮中央7毫米后,用光敏剂核黄素和3A紫外线辐照度(370 nm UVA)在3 mW / cm2的辐照度下对角膜进行30分钟的处理。治疗后立即分别在3个月和8个月处死三只动物。使用微型计算机控制的生物材料测试仪在4 x 10毫米的角膜条上进行生物力学应力应变测量。结果:处理过的兔角膜的角膜厚度为408±20毫米。在长达8个时间段内,发现极限应力(69.7-106.0%)恒定,显着增加,杨氏弹性模量(78.4-87.4%)和极限应变减小(0.57-78.4%)。结论:核黄素/ UVA诱导的胶原蛋白交联导致生物力学刚度长期增加,并随着时间的推移保持稳定。这些数据支持了我们先前的长期临床观察,并希望这种新的治疗方法能够最终阻止圆锥角膜的进展。

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