Abstract

Modification of cerebral perfusion pressure and cerebral blood flow (CBF) are crucial components of the therapies designed to reduce secondary damage after traumatic brain injury (TBI). Previously we documented a robust decrease in CBF after rapid sagittal head rotation in our well-validated animal model of diffuse TBI. Mechanisms responsible for this immediate (<10 min) and sustained (∼24 h) reduction in CBF have not been explored. Because the carotid arteries are a major source of CBF, we hypothesized that blood flow through the carotid arteries (Q) and vessel diameter (D) would decrease after rapid nonimpact head rotation without cervical spine injury. Four-week-old (toddler) female piglets underwent rapid (<20 msec) sagittal head rotation without impact, previously shown to produce diffuse TBI with reductions in CBF. Ultrasonographic images of the bilateral carotid arteries were recorded at baseline (pre-injury), as well as immediately after head rotation and 15, 30, 45, and 60 min after injury. Diameter (D) and waveform velocity (V) were used to calculate blood flow (Q) through the carotid arteries using the equation Q=(0.25)πD(2)V. D, V, and Q were normalized to the pre-injury baseline values to obtain a relative change after injury in right and left carotid arteries. Three-way analysis of variance and post-hoc Tukey-Kramer analyses were used to assess statistical significance of injury, time, and side. The relative change in carotid artery diameter and flow was significantly decreased in injured animals in comparison with uninjured sham controls (p<0.0001 and p=0.0093, respectively) and did not vary with side (p>0.39). The average carotid blood velocity did not differ between sham and injured animals (p=0.91). These data suggest that a reduction in global CBF after rapid sagittal head rotation may be partially mediated by a reduction in carotid artery flow, via vasoconstriction.

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