Temporal Profile of Cortical Perfusion and Microcirculation after Controlled Cortical Impact Injury in Rats

Abstract

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.

Cerebral Blood Volume Alterations in the Perilesional Areas in the Rat Brain after Traumatic Brain Injury—Comparison with Behavioral Outcome

“…Interpretation of decreased CBV as a hypoperfusion immediately after TBI seems reasonable, because the CBV and CBF have been shown to be linked in experimental studies of TBI in acute phase (Prat et al, 1997;Thomale et al, 2002). Furthermore, we observed CBV drop during the first hours after head trauma, at the time when decrease in perfusion (CBF) has been well documented by several research groups (Prat et al, 1997;Thomale et al, 2002;Ginsberg et al, 1997;Bryan et al, 1995). Similarly, we attributed the increased CBV in the hippocampus in subacute phase to increased CBF.…”

“…Marked decrease in CBV and CBF has been found 3 to 4 h after injury in the rat model of closed head injury (Prat et al, 1997;Thomale et al, 2002). Local CBF has been found to decrease 15 mins after injury and remain decreased up to 4 h in lateral fluid percussion rat models (Ginsberg et al, 1997) and similar patter of CBF has been found in humans Kelly et al, 1996Kelly et al, , 1997.…”

“…The CBF studies in this rat model report acute hypoperfusion followed by hyperperfusion up till 48 h (Thomale et al, 2002). However, the temporal patterns of CBV alterations starting on acute phase after injury and extending to the subacute phase, i.e., several days/weeks after injury have not been studied.…”

Development of Magnetic Resonance Imaging Biomarkers for Traumatic Brain Injury

“…Thomale et al showed that the acute hypoperfusion after TBI is due to vasoconstriction (Thomale et al 2002). This study also found hyperemia occurring between 24 and 48 h after TBI in the controlled cortical impact model using LDF.…”

“…Ultrastructural alterations in the lumen and wall of sensorimotor cortical microvessels, including endothelial cell distortion and luminal collapse, were seen between 1 and 48 h after trauma. Smooth muscle in the wall of reacting microvessels showed evidence of increased contractility that coincided temporally with the decreased perfusion of cortical CBF.Thomale et al showed that the acute hypoperfusion after TBI is due to vasoconstriction (Thomale et al 2002). This study also found hyperemia occurring between 24 and 48 h after TBI in the controlled cortical impact model using LDF.…”