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

Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine

Marc Maegele¹  Qiaobing Huang²  Edmund Neugebauer³  Yongjun Yuan²  Manuel Mutschler¹  Bo Chen² 

[1] Department of Traumatology, Orthopedic Surgery and Sportsmedicine, Private University of Witten-Herdecke, Cologne-Merheim Medical Center (CMMC), Ostmerheimerstr. 200, D-51109 Cologne, Germany;Department of Pathophysiology, Key Laboratory for Shock and Microcirculation Research, Southern Medical University (SMU), Tong He, 510515 Guangzhou, People's Republic of China;Institute for Research in Operative Medicine (IFOM), Private University of Witten-Herdecke, Cologne Merheim Medical Center (CMMC), Ostmerheimerstr. 200, D-51109 Cologne, Germany

关键词: Microcirculation;    Vasomotor response;    Third order vessels;    Spinotrapezius muscle;    Brain injury;    Lateral fluid percussion;    Hemorrhagic shock;    Trauma;   

Others  :  810641
DOI  :  10.1186/1757-7241-21-77

 received in 2013-09-23, accepted in 2013-11-18,  发布年份 2013

【 摘 要 】

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.

【 授权许可】

   
2013 Chen et al.; licensee BioMed Central Ltd.

【 图 表 】

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