Effects of ultrasonic vibration on the microstructure and mechanical properties of high alloying TiAl

• Published in: Scientific reports Vol. 7; no. 1; p. 41463
• Main Authors: Ruirun, Chen, Deshuang, Zheng, Tengfei, Ma, Hongsheng, Ding, Yanqing, Su, Jingjie, Guo, Hengzhi, Fu
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 24.01.2017; Nature Publishing Group
• Subjects: 639/301/1023/1026; 639/766/25/3927; Alloys; Cavitation; Chemical composition; Colonies; Humanities and Social Sciences; Mechanical properties; Microstructure; multidisciplinary; Nucleation; Science; Vibration
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/srep41463

To modify the microstructure and enhance performances, the ultrasonic vibration is applied in the mould casting of TiAl alloy. The effects and mechanism of ultrasonic vibration on the solidifying microstructure and mechanical properties are investigated and the model for predicting lamellar colony size is established. After ultrasonic vibration, the coarse microstructure is well modified and lamellar colony is refined from 534 μm to 56 μm. Most of precipitated phases are dissolved into the lamellar colony leading to a homogenous element distribution. The phase ratio of α 2 -Ti 3 Al and γ -TiAl is increased, and the chemical composition is promoted to more close to equilibrium level by weakening the influence of β -alloying elements. The microhardness and yield strength are gradually improved by 23.72% and 181.88% due to the fine grain strengthening, while the compressive strength is enhanced by 24.47% through solution strengthening. The critical ultrasonic intensity ( I b ) for TiAl alloy is estimated at 220 W cm −2 and the model for average lamellar colony size is established as . The ultrasonic refinement efficiency exponentially increases as the ultrasonic vibration time with a theoretic limit maximum value of E lim  = 88% and the dominating refinement mechanism by ultrasonic vibration is the cavitation-enhanced nucleation rather than cavitation-induced dendrite fragmentation.