Fig. 7. Acute cellular permeability increases in vitro depend on mode of bulk loading. Representative confocal reconstructions of calcein+ cells following static control conditions or mechanical loading (0.50 strain at 1, 10, or 30 s-1 strain rate). Calcein, a normally cell-impermeant molecule, was added to the extracellular space prior to loading but becomes intracellularly sequestered following loading. Reconstructions from 50 mm thick z-stacks are shown here.

failure at the cellular level. Models of neural trauma that represent the related biomechanics and pathophysiology are important for the elucidation of cellular tolerances and the development of mechanistically driven intervention strategies.

Secondary response

Primary damage initiates a cascade of secondary responses, leading to cell death, network dysfunction, and system-level changes (Fig. 8). While there is no absolute time when primary damage evolves into delayed effects, the secondary phase of injury can be defined as any consequence of the primary insult. This may be in the acute (minutes to hours) period or in a more delayed fashion (days to months) and is dependent on the severity of the initial insult, as well as the health and age of the individual. There is a role for biomechanics in determining injury mechanisms in both the primary and secondary phases of the injury response by utilizing laboratory models that best mimic the forces/stresses and deformations/strains that occur during a traumatic insult. The response (whether cellular or whole organism) can better represent the clinical setting and therefore potential treatments can be evaluated in a more relevant setting.

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