Controlled inertial loading of the head was used in an experimental setting producing varying degrees of ischemic changes in the brains of subhuman primates. Sampling from frozen coronal sections of the brain enables one to quantitate the ATP levels of the local specimens and, subsequently, to map the topographical distribution of this biochemical indicator of ischemia.
In parallel with the subhuman primate studies a series of physical model experiments were conducted in order to estimate the magnitude of the strains produced throughout the surrogate brain material under identical loading conditions. Based upon isolated vascular tissue experiments we have been able to demonstrate a strain-dependent vasoconsuiction that occurs in the vessel under conditions of high strain rate extension. We, therefore, hypothesized regional changes in cerebral blood flow would accompany changes in the strain field.
We have mapped the strain field onto the topographic distribution of the alterations in ATP levels and have demonstrated a correlation between the magnitude of the principal strains and the degree of ischemic change. This finding should be considered in the context of the development of improved head injury tolerance criteria, in that a threshold exists for ischemic brain damage as a function of acceleration of the head through the mechanism of strain-dependent vasoreactivity.