Superimposed traumatic brain injury modulates vasomotor responses in third-order vessels
after hemorrhagic shock
Sammanfattning
BACKGROUND:
Traumatic brain injury (TBI) and hemorrhagic shock (HS) are the leading causes of death in trauma.
Recent studies suggest that TBI may influence physiological responses to acute blood loss. This
study was designed to assess to what extent superimposed TBI may modulate physiologic
vasomotor responses in third-order blood vessels in the context of HS.
METHODS:
We have combined two established experimental models of pressure-controlled hemorrhagic shock
(HS; MAP 50 mmHg/60 min) and TBI (lateral fluid percussion (LFP)) to assess vasomotor responses
and microcirculatory changes in third-order vessels by intravital microscopy in a spinotrapezius
muscle preparation. 23 male Sprague-Dawley rats (260-320 g) were randomly assigned to
experimental groups: i) Sham, ii) HS, iii) TBI + HS, subjected to impact or sham operation, and
assessed.
RESULTS:
HS led to a significant decrease in arteriolar diameters by 20% to baseline (p < 0.01). In TBI + HS this
vasoconstriction was less pronounced (5%, non-significant). At completed and at 60 minutes of
resuscitation arteriolar diameters had recovered to pre-injury baseline values. Assessment of
venular diameters revealed similar results. Arteriolar and venular RBC velocity and blood flow
decreased sharply to < 20% of baseline in HS and TBI + HS (p < 0.01). Immediately after and at 60
minutes of resuscitation, an overshoot in arterial RBC velocity (140% of baseline) and blood flow
(134.2%) was observed in TBI + HS.
CONCLUSION:
Superimposed TBI modulated arteriolar and venular responses to HS in third-order vessels in a
spinotrapezius muscle preparation. Further research is necessary to precisely define the role of TBI
on the microcirculation in tissues vulnerable to HS.