Superimposed traumatic brain injury modulates vasomotor responses in third-order vessels after hemorrhagic shock

Bo Chen,Yongjun Yuan,Marc Maegele,Qiaobing Huang,Manuel Mutschler,Edmund Neugebauer

doi:10.1186/1757-7241-21-77

Abstract

BackgroundTraumatic 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.MethodsWe 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.ResultsHS 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.ConclusionSuperimposed 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.

Highlights

Traumatic brain injury (TBI) and hemorrhagic shock (HS) are the leading causes of death in trauma
Mean arterial blood pressure (MAP) and mortality All animals included in this study were comparable at baseline for size, weight, haemoglobin and pH values
There were no differences in mean arterial blood pressure (MAP) curves observed between HS only and TBI + HS groups (Figure 3)

Summary

Introduction

Traumatic brain injury (TBI) and hemorrhagic shock (HS) are the leading causes of death in trauma. Several studies have shown that superimposed TBI to hemorrhage, In order to maintain tissue perfusion and to preserve physiological hemodynamics, an adequate function of the peripheral microcirculation within the different organ systems is fundamental [14]. Extracranial hemorrhage is known to be associated with microcirculatory hypoperfusion and subsequent tissue damage by inducing vasoconstriction and decreasing arterial blood flow [15,16,17]. This microcirculatory response to extracranial hemorrhage when coincidenced with a superimposed TBI, as frequently encountered in the clinical setting, is yet to be defined. Several studies have demonstrated that various models of TBI may create an acute and transient systemic hypertension and bradycardia which is followed by a hypodynamic state with heterogeneous hypoperfusion among organs at increasing magnitudes of injury [18,19]

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