scholarly journals Hemorrhagic Shock after Experimental Traumatic Brain Injury in Mice: Effect on Neuronal Death

2009 ◽  
Vol 26 (6) ◽  
pp. 889-899 ◽  
Author(s):  
Alia Marie Dennis ◽  
M. Lee Haselkorn ◽  
Vincent A. Vagni ◽  
Robert H. Garman ◽  
Keri Janesko-Feldman ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hemorrhagic Shock ◽  
Neuronal Death ◽  
Experimental Traumatic Brain Injury

EFFECT OF HEMORRHAGIC SHOCK ON NEURONAL DEATH AFTER EXPERIMENTAL TRAUMATIC BRAIN INJURY IN MICE.

2006 ◽  
Vol 34 ◽  
pp. A17
Author(s):  
M L Haselkorn ◽  
Alia Marie Dennis ◽  
Vincent Vagni ◽  
Keri Janesko-Feldman ◽  
Robert S Clark ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hemorrhagic Shock ◽  
Neuronal Death ◽  
Experimental Traumatic Brain Injury

scholarly journals Hemorrhagic Shock Shifts the Serum Cytokine Profile from Pro- to Anti-Inflammatory after Experimental Traumatic Brain Injury in Mice

2014 ◽  
Vol 31 (16) ◽  
pp. 1386-1395 ◽  
Author(s):  
Steven L. Shein ◽  
David K. Shellington ◽  
Jennifer L. Exo ◽  
Travis C. Jackson ◽  
Stephen R. Wisniewski ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hemorrhagic Shock ◽  
Cytokine Profile ◽  
Serum Cytokine ◽  
Anti Inflammatory ◽  
Experimental Traumatic Brain Injury

scholarly journals Mri Assessment of Cerebral Blood Flow after Experimental Traumatic Brain Injury Combined with Hemorrhagic Shock in Mice

2012 ◽  
Vol 33 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Lesley M Foley ◽  
Alia M Iqbal O'Meara ◽  
Stephen R Wisniewski ◽  
T Kevin Hitchens ◽  
John A Melick ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Hemorrhagic Shock ◽  
Neuronal Death ◽  
Mouse Strains ◽  
Combined Injury ◽  
Injury Model ◽  
The Impact

Secondary insults such as hypotension or hemorrhagic shock (HS) can greatly worsen outcome after traumatic brain injury (TBI). We recently developed a mouse combined injury model of TBI and HS using a controlled cortical impact (CCI) model and showed that 90 minutes of HS can exacerbate neuronal death in hippocampus beneath the contusion. This combined injury model has three clinically relevant phases, a shock, pre hospital, and definitive care phases. Mice were randomly assigned to four groups, shams as well as a CCI only, an HS only, and a CCI + HS groups. The CCI and HS reduced cerebral blood flow (CBF) in multiple regions of interest (ROIs) in the hemisphere ipsilateral and contralateral to injury. Hemorrhagic shock to a level of ~30 mm Hg exacerbated the CCI-induced CBF reductions in multiple ROIs ipsilateral to injury (hemisphere and thalamus) and in the hemisphere contralateral to injury (hemisphere, thalamus, hippocampus, and cortex, all P < 0.05 versus CCI only, HS only or both). An important effect of HS duration was also seen after CCI with maximal CBF reduction seen at 90 minutes ( P < 0.0001 group-time effect in ipsilateral hippocampus). Given that neuronal death in hippocampus is exacerbated by 90 minutes of HS in this model, our data suggest an important role for exacerbation of posttraumatic ischemia in mediating the secondary injury in CCI plus HS. In conclusion, the serial, non invasive assessment of CBF using ASL-MRI (magnetic resonance imaging with arterial spin labeling) is feasible in mice even in the complex setting of combined CCI + HS. The impact of resuscitation therapies and various mutant mouse strains on CBF and other outcomes merits investigation in this model.

Effects of ethanol on brain lactate in experimental traumatic brain injury with hemorrhagic shock

1999 ◽  
Vol 837 (1-2) ◽  
pp. 1-7 ◽  
Author(s):  
Brian J. Zink ◽  
Carol H. Schultz ◽  
Xu Wang ◽  
Michelle Mertz ◽  
Susan A. Stern ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hemorrhagic Shock ◽  
Experimental Traumatic Brain Injury ◽  
Brain Lactate

scholarly journals Polynitroxylated-Pegylated Hemoglobin Attenuates Fluid Requirements and Brain Edema in Combined Traumatic Brain Injury Plus Hemorrhagic Shock in Mice

2013 ◽  
Vol 33 (9) ◽  
pp. 1457-1464 ◽  
Author(s):  
Erik C Brockman ◽  
Hülya Bayir ◽  
Brian Blasiole ◽  
Steven L Shein ◽  
Ericka L Fink ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Hemorrhagic Shock ◽  
Brain Edema ◽  
Dry Weight ◽  
Bovine Hemoglobin ◽  
Shed Blood ◽  
Brain Water ◽  
Experimental Traumatic Brain Injury

Polynitroxylated-pegylated hemoglobin (PNPH), a bovine hemoglobin decorated with nitroxide and polyethylene glycol moieties, showed neuroprotection vs. lactated Ringer’s (LR) in experimental traumatic brain injury plus hemorrhagic shock (TBI + HS). Hypothesis: Resuscitation with PNPH will reduce intracranial pressure (ICP) and brain edema and improve cerebral perfusion pressure (CPP) vs. LR in experimental TBI + HS. C57/BL6 mice ( n = 20) underwent controlled cortical impact followed by severe HS to mean arterial pressure (MAP) of 25 to 27 mm Hg for 35 minutes. Mice ( n = 10/group) were then resuscitated with a 20 mL/kg bolus of 4% PNPH or LR followed by 10 mL/kg boluses targeting MAP > 70 mm Hg for 90 minutes. Shed blood was then reinfused. Intracranial pressure was monitored. Mice were killed and %brain water (%BW) was measured (wet/dry weight). Mice resuscitated with PNPH vs. LR required less fluid (26.0 ± 0.0 vs. 167.0 ± 10.7 mL/kg, P < 0.001) and had a higher MAP (79.4 ± 0.40 vs. 59.7 ± 0.83 mm Hg, P < 0.001). The PNPH-treated mice required only 20 mL/kg while LR-resuscitated mice required multiple boluses. The PNPH-treated mice had a lower peak ICP (14.5 ± 0.97 vs. 19.7 ± 1.12 mm Hg, P = 0.002), higher CPP during resuscitation (69.2 ± 0.46 vs. 45.5 ± 0.68 mm Hg, P < 0.001), and lower %BW vs. LR (80.3 ± 0.12 vs. 80.9 ± 0.12%, P = 0.003). After TBI + HS, resuscitation with PNPH lowers fluid requirements, improves ICP and CPP, and reduces brain edema vs. LR, supporting its development.

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