Background: Traumatic brain injury (TBI) and hemorrhagic shock (HS) are the leading causes of death in trauma.\r\nRecent studies suggest that TBI may influence physiological responses to acute blood loss. This study was designed\r\nto assess to what extent superimposed TBI may modulate physiologic vasomotor responses in third-order blood\r\nvessels in the context of HS.\r\nMethods: We have combined two established experimental models of pressure-controlled hemorrhagic shock\r\n(HS; MAP 50 mmHg/60 min) and TBI (lateral fluid percussion (LFP)) to assess vasomotor responses and microcirculatory\r\nchanges in third-order vessels by intravital microscopy in a spinotrapezius muscle preparation. 23 male Spragueââ?¬â??\r\nDawley rats (260ââ?¬â??320 g) were randomly assigned to experimental groups: i) Sham, ii) HS, iii) TBI + HS, subjected to\r\nimpact or sham operation, and assessed.\r\nResults: HS led to a significant decrease in arteriolar diameters by 20% to baseline (p < 0.01). In TBI + HS this\r\nvasoconstriction was less pronounced (5%, non-significant). At completed and at 60 minutes of resuscitation arteriolar\r\ndiameters had recovered to pre-injury baseline values. Assessment of venular diameters revealed similar results.\r\nArteriolar and venular RBC velocity and blood flow decreased sharply to < 20% of baseline in HS and TBI + HS\r\n(p < 0.01). Immediately after and at 60 minutes of resuscitation, an overshoot in arterial RBC velocity (140% of baseline)\r\nand blood flow (134.2%) was observed in TBI + HS.\r\nConclusion: Superimposed TBI modulated arteriolar and venular responses to HS in third-order vessels in a spinotrapezius\r\nmuscle preparation. Further research is necessary to precisely define the role of TBI on the microcirculation in tissues\r\nvulnerable to HS.
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