Miller D L
Ultrasound Med Biol. 1985 Mar-Apr;11(2):285-92. doi: 10.1016/0301-5629(85)90127-9.
The hypothesis that ultrasonically induced membrane damage and cell death in Elodea leaves is caused by shear stress associated with microstreaming flow generated in the vicinity of oscillating gas-filled channels between the cells is investigated. Cell death thresholds as a function of frequency seem to follow a condition of constant shear stress, with minimum thresholds near the resonance frequency of a gas-filled channel. Theoretical estimates of the shear stress generated within the cells at the ultrasonic intensity of the cell death threshold are in order of magnitude agreement with measurements of the shear stress required for lysis of blood cells. Furthermore, the dependence of the cell death thresholds on exposure duration seems to correspond roughly with the dependence of critical shear stress for blood cells as a function of the duration of the stress. Membrane damage induced by microstreaming shear stress therefore appears to be a plausible mechanism of cell death in Elodea, and a valuable unifying concept for consideration of bioeffects of ultrasonic cavitation.
研究了关于伊乐藻叶片中超声诱导的膜损伤和细胞死亡是由与细胞间振荡充气通道附近产生的微流引起的剪切应力所致的假说。细胞死亡阈值作为频率的函数似乎遵循恒定剪切应力条件，在充气通道的共振频率附近阈值最低。在细胞死亡阈值的超声强度下，细胞内产生的剪切应力的理论估计值与血细胞裂解所需剪切应力的测量值在数量级上一致。此外，细胞死亡阈值对暴露持续时间的依赖性似乎大致与血细胞临界剪切应力对应力持续时间的依赖性相对应。因此，微流剪切应力诱导的膜损伤似乎是伊乐藻细胞死亡的一种合理机制，也是考虑超声空化生物效应的一个有价值的统一概念。
