Sub-50-fs laser retinal damage thresholds in primate eyes with group velocity dispersion, self-focusing and low-density plasmas
Sub-50-fs laser retinal damage thresholds in primate eyes with group velocity dispersion, self-focusing and low-density plasmas
复制标题
DOI：
10.1007/s00417-004-0924-9
复制
发表时间：
2005-02-01
影响因子：
2.7
通讯作者：
Rockwell, BA
中科院分区：
文献类型：
--
作者：
Cain, CP;Thomas, RJ;Rockwell, BA
背景：使用近红外亚 50 飞秒激光脉冲进行体内视网膜损伤研究必须考虑非线性效应，例如群速度色散 (GVD)、自聚焦、激光诱导击穿 (LIB) 和低密度等离子体 (LDP)。在本文中，我们介绍了非线性效应的理论计算结果以及活体眼睛可见损伤阈值的实验测量结果。我们将这些值与人工眼中测得的 LIB 和 LDP 阈值进行比较。所有三个阈值均在使用或不使用预啁啾输入脉冲以补偿 GVD 效应的情况下进行测量。方法：我们记录了亚 50 飞秒激光脉冲的体内最小可见损伤 (MVL) 阈值，无论是否对输入脉冲进行预啁啾。此外，我们还在人工眼内测量了有或没有预啁啾的 LIB 和 LDP 阈值。需要不同程度的预啁啾才能对活体眼和人造眼中的 GVD 进行最佳补偿。对所有数据进行概率分析，并对阈值进行比较，以确定对 GVD 线性调频补偿的三个阈值的影响。结果：我们将 GVD 补偿、自聚焦、LIB 和低密度等离子体的非线性建模和计算结果与我们使用活体眼睛和人造眼的实验结果进行了比较。使用最佳啁啾脉冲时，活体眼睛的损伤阈值能量从平相位输入的 0.25 muJ 下降到 0.17 muJ，而使用最佳啁啾脉冲时，LIB 阈值从 0.29 muJ 降低到 0.19 muJ。通过预啁啾脉冲，LDP 阈值从 0.21 muJ 下降到 0.14 muJ。在 44 fs 时，这些能量产生的峰值功率至少是计算出的临界功率的两倍，该临界功率会产生非线性自聚焦和光束塌陷，以便在均匀介质中传播无畸变高斯光束。结论：根据我们对有或没有 GVD 补偿的 MVL 阈值的测量，我们得出结论，由于 GVD，恒河猴眼中 44 fs 脉冲产生的可见损伤阈值的能量增加。当脉冲被预啁啾以补偿眼睛中的 GVD 时，MVL ED50 减少了三分之一。当使用预啁啾脉冲与非啁啾脉冲时，这种幅度的减小也适用于 LIB ED50 气泡阈值和 LDP ED50 等离子体通道的人工眼。我们还从提供的数据中得出结论，对于 50 fs 及以下的脉冲持续时间，低密度等离子体（而不是 LIB 空化气泡）是在活体眼睛内观察到的可见损伤阈值的可能中介因素。因此，在这些脉冲持续时间的 MVL 阈值能量下，LDP 创建的等离子体通道即使不是唯一的损伤机制，也是主要的损伤机制。
Background: In vivo retinal injury studies using sub-50-femtosecond laser pulses in the near-infrared must consider nonlinear effects such as group velocity dispersion (GVD), self-focusing, laser-induced breakdown (LIB) and low-density plasmas (LDPs). In this paper we present the results of our theoretical calculations of nonlinear effects and our experimental measurements for the visible lesion thresholds in live eyes. We compare these values with the measured LIB and LDP thresholds in an artificial eye. All three thresholds were measured with and without pre-chirping the input pulse to compensate for GVD effects. Methods: We recorded the minimum visible lesion (MVL) thresholds in vivo for sub-50-fs laser pulses, with and without pre-chirping the input pulses. In addition, we measured the LIB and LDP thresholds, with and without pre-chirping, within an artificial eye. Different degrees of pre-chirping were required to give optimal compensation for GVD in the live eye and the artificial eye. Probit analysis was used on all data, and comparisons among thresholds were made, to determine the effects on the three thresholds of chirp compensation for GVD. Results: Results of our nonlinear modeling and calculations for GVD compensation, self-focusing, LIB, and low-density plasmas were compared with our experimental results using live eyes and the artificial eye. The damage threshold in live eyes dropped in energy from 0.25 muJ, for the flat-phase input, to 0.17 muJ when optimally chirped pulses were used, while the LIB threshold was reduced from 0.29 muJ to 0.19 muJ with optimally chirped pulses. The LDP threshold dropped from 0.21 muJ to 0.14 muJ with the pre-chirped pulse. At 44 fs, these energies produced peak powers at least twice the calculated critical power that produces nonlinear self-focusing and beam collapse, for propagation of non-aberrated gaussian beams in a uniform medium. Conclusions: Based on our measurements of the MVL thresholds, with and without GVD compensation, we conclude that the visible lesion thresholds produced by 44 fs pulses in rhesus eyes are increased in energy due to GVD. The MVL ED50 was reduced by one third when the pulse was pre-chirped to compensate for GVD in the eye. This reduction in amplitude also holds true in the artificial eye for the LIB ED50 bubble thresholds and the LDP ED50 plasma channels, when using pre-chirped pulses versus non-chirped pulses. We also conclude from the data presented that low-density plasmas, and not LIB cavitation bubbles, are the probable mediating factor at the visible lesion thresholds observed within live eyes, for pulse durations at and below 50 fs. Therefore, the plasma channel created by LDPs is the major damage mechanism, if not the only damage mechanism, at MVL threshold energies for these pulse durations.