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Retardation and repair of fatigue cracks in a microcapsule toughened epoxy composite-Part II: In situ self-healing

机译:微胶囊增韧环氧复合材料疲劳裂纹的延缓和修复-第二部分:原位自修复

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Successful arrest and retardation of fatigue cracks is achieved with an in situ self-healing epoxy matrix composite that incorporates microencapsulated dicyclopentadiene (DCPD) healing agent and Grubbs' first generation Ru catalyst. Healing agent is released into the crack plane by the propagating crack, where it polymerizes to form a polymer wedge, generating a crack tip shielding mechanism. Due to the complex kinetics of healing a growing crack, the resulting in situ retardation and arrest of fatigue cracks exhibit a strong dependence on the applied range of cyclic stress intensity DELTA K_I. Significant crack arrest and life-extension result when the in situ healing rate is faster than the crack growth rate. In loading cases where the crack grows too rapidly (maximum applied stress intensity factor is a significant percentage of the mode-I fracture toughness value), a carefully timed rest period can be used to prolong fatigue life up to 118 percent. At moderate DELTA K_I, in situ healing extends fatigue life by as much as 213 percent. Further improvements in fatigue life-extension are achieved by employing a rest period, which leads to permanent arrest at this moderate DELTA K_I. At lower values of applied stress intensity factor, self-healing yields complete arrest of fatigue cracks providing infinite fatigue life-extension.
机译:现场裂纹的成功修复和延迟是通过采用原位自修复环氧基质复合材料实现的,该复合材料结合了微囊化的双环戊二烯(DCPD)固化剂和Grubbs的第一代Ru催化剂。愈合剂通过扩展的裂缝释放到裂缝平面中,在此处聚合形成聚合物楔,从而产生裂缝尖端的屏蔽机制。由于修复不断增长的裂纹的复杂动力学,导致的疲劳裂纹的原位阻滞和滞留表现出对循环应力强度DELTA K_I的应用范围的强烈依赖。当原位愈合速度快于裂纹生长速度时,会导致明显的裂纹停止和寿命延长。在裂纹增长过快的加载情况下(最大施加应力强度因子是I型断裂韧性值的很大百分比),可以使用精心安排的定时休息时间将疲劳寿命延长至118%。在中等DELTA K_I下,原位愈合可将疲劳寿命延长213%。通过使用休息时间,可以进一步延长疲劳寿命,从而导致在此中等DELTA K_I下永久性停滞。在较低的施加应力强度因子值下,自愈可完全阻止疲劳裂纹,从而无限延长疲劳寿命。

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