Cavitation nucleation and its ductile-to-brittle shape transition in soft gels under translational mechanical impact

Abstract

Cavitation bubbles in the human body, when subjected to impact, are being increasingly considered as a possible brain injury mechanism. However, the onset of cavitation and its complex dynamics in biological materials remain unclear. Our experimental results using soft gels as a tissue simulant show that the critical acceleration (acr) at cavitation nucleation monotonically increases with increasing stiffness of gelatin A/B, while acr for agarose and agar initially increases but is followed by a plateau or even decrease after stiffness reach to ∼100 kPa. Our image analyses of cavitation bubbles and theoretical work reveal that the observed trends in acr are directly linked to how bubbles grow in each gel. Gelatin A/B, regardless of their stiffness, form a localized damaged zone (tens of nanometers) at the gel-bubble interface during bubble growth. In contrary, the damaged zone in agar/agarose becomes significantly larger (> 100 times) with increasing shear modulus, which triggers the transition from formation of a small, damaged zone to activation of crack propagation. Statement of SignificanceWe have studied cavitation nucleation and bubble growth in four different types of soft gels (i.e., tissue simulants) under translational impact. The critical linear acceleration for cavitation nucleation has been measured in the simulants by utilizing a recently developed method that mimics acceleration profiles of typical head blunt events. Each gel type exhibits significantly different trends in the critical acceleration and bubble shape (e.g., A gel-specific sphere-to-saucer transition) with increasing gel stiffness. Our theoretical framework, based on the concepts of a damaged zone and crack propagation in each gel, explains underlying mechanisms of the experimental observations. Our in-depth studies shed light on potential links between traumatic brain injuries and cavitation bubbles induced by translational acceleration, the overlooked mechanism in the literature.