Central nervous system trauma is a major public health problem. In order to study the effects of this trauma on the neural and vascular tissues of the brain requires examining the response of its individual components. This necessitates generation of failure criteria which deal with the physiology of the system rather than the structure. The use of a cellular model provides a method for broadening the definition of failure and concurrently uncovering the fundamental processes of trauma.
The functional and structural effects of uniaxial loading on a isolated neural tissue were studied using the giant axon of the squid Loligo Pealei. An apparatus capable of applying controlled loads to a viable, isolated tissue and monitoring its physiological response was designed. While essentially a material testing device with appropriate stimulating and recording electrodes, it also provided an atraumatic, uniformly distributed specimen grip, and a controlled intra and extracellular environment. The system produced programmable displacements and stimuli, while simultaneously monitoring input displacement, resultant force, and either membrane potential or current. Loading regimes of quasi-static ramp, damped exponential pulse, step or oscillatory waveforms were employed.
The axon's constitutive properties are similar to other nonlinear soft tissues whose stiffness increase with deformation. Although quasi-static loading failed to produce an electrophysiological effect, an increase in the loading rate resulted in graded membrane depolarizations which were a function of strain and strain rate. Below extensions of ten percent, these perturbations were transient and recovered to preinsult levels over the course of several minutes. Stretches above this level however, resulted in incomplete recovery of membrane potential to its resting value, and structural failure occurred at twenty five percent strain. This state of functional imparement which occurs as a result of deformation suggests alterations in membrane permeability and a conceptual model of the process is presented.
This research has produced an isolated tissue model of neural injury as a function of high strain rate uniaxial extension. By using membrane potential as a determiner of injury, the data is shown to correlate with the clinically observed spectrum of dysfunction in terms of both severity and time course.