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Impaired cerebral perfusion contributes to evolving posttraumatic tissue damage. Spontaneous reversibility of reduced perfusion within the first days after injury could make a persisting impact on secondary tissue damage less likely and needs to be considered for possible therapeutic approaches. The present study was designed to characterize the temporal profile and impact of trauma severity on cortical perfusion and microcirculation during the first 48 h after controlled cortical impact injury (CCI). In 10 rats, pericontusional cortical perfusion and microcirculation using laser Doppler flowmetry (LDF) and orthogonal polarization spectral (OPS) imaging were assessed before, and at 4, 24, and 48 h after CCI. Influence of trauma severity was studied by varying the penetration depth of the impactor rod (0.5 vs. 1 mm), thereby inducing a less and a more severe contusion. Mean arterial blood pressure (MABP), arterial blood gases, and blood glucose were monitored. With unchanged MABP and paCO2, cortical perfusion and microcirculation were significantly impaired during the first 48 h following CCI. Hypoperfusion observed at 4 h related to vasoconstriction and microcirculatory stasis preceded a long-lasting phase of hyperperfusion at 24 and 48 h reflected by vasodilation and increased flow velocity in arterioles and venules. Hyperperfusion was mostly pronounced in rats with a less severe contusion. Following CCI, trauma severity markedly influences changes in pericontusional cortical perfusion and microcirculation. Overall, pericontusional cortical hypoperfusion observed within the early phase preceded a long lasting phase of hyperperfusion up to 48 h after CCI.
Thomale et al. (Mon,) studied this question.