scholarly journals Resuscitation of Traumatic Brain Injury and Hemorrhagic Shock with Polynitroxylated Albumin, Hextend, Hypertonic Saline, and Lactated Ringer's: Effects on Acute Hemodynamics, Survival, and Neuronal Death in Mice

2009 ◽  
Vol 26 (12) ◽  
pp. 2403-2408 ◽  
Author(s):  
Jennifer L. Exo ◽  
David K. Shellington ◽  
Hülya Bayır ◽  
Vincent A. Vagni ◽  
Keri Janesco-Feldman ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hemorrhagic Shock ◽  
Hypertonic Saline ◽  
Neuronal Death

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

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.

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

Hypertonic saline in traumatic brain injury: Current status

2004 ◽  
Vol 1 (2) ◽  
pp. 15-20 ◽  
Author(s):  
Kavita Sandhu ◽  
TVSP Murthy ◽  
Brig T Prabhakar
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hypertonic Saline ◽  
Current Status

scholarly journals Resuscitation from hemorrhagic shock after traumatic brain injury with polymerized hemoglobin

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cynthia R. Muller ◽  
Vasiliki Courelli ◽  
Alfredo Lucas ◽  
Alexander T. Williams ◽  
Joyce B. Li ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hemorrhagic Shock ◽  
Ischemia Reperfusion Injury ◽  
Diastolic Pressure ◽  
Ischemia Reperfusion ◽  
Treatment Strategies ◽  
Secondary Bleeding ◽  
Additional Testing ◽  
Systolic Blood Pressure Variability

AbstractTraumatic brain injury (TBI) is often accompanied by hemorrhage, and treatment of hemorrhagic shock (HS) after TBI is particularly challenging because the two therapeutic treatment strategies for TBI and HS often conflict. Ischemia/reperfusion injury from HS resuscitation can be exaggerated by TBI-induced loss of autoregulation. In HS resuscitation, the goal is to restore lost blood volume, while in the treatment of TBI the priority is focused on maintenance of adequate cerebral perfusion pressure and avoidance of secondary bleeding. In this study, we investigate the responses to resuscitation from severe HS after TBI in rats, using fresh blood, polymerized human hemoglobin (PolyhHb), and lactated Ringer’s (LR). Rats were subjected to TBI by pneumatic controlled cortical impact. Shortly after TBI, HS was induced by blood withdrawal to reduce mean arterial pressure (MAP) to 35–40 mmHg for 90 min before resuscitation. Resuscitation fluids were delivered to restore MAP to ~ 65 mmHg and animals were monitored for 120 min. Increased systolic blood pressure variability (SBPV) confirmed TBI-induced loss of autoregulation. MAP after resuscitation was significantly higher in the blood and PolyhHb groups compared to the LR group. Furthermore, blood and PolyhHb restored diastolic pressure, while this remained depressed for the LR group, indicating a loss of vascular tone. Lactate increased in all groups during HS, and only returned to baseline level in the blood reperfused group. The PolyhHb group possessed lower SBPV compared to LR and blood groups. Finally, sympathetic nervous system (SNS) modulation was higher for the LR group and lower for the PolyhHb group compared to the blood group after reperfusion. In conclusion, our results suggest that PolyhHb could be an alternative to blood for resuscitation from HS after TBI when blood is not available, assuming additional testing demonstrate similar favorable results. PolyhHb restored hemodynamics and oxygen delivery, without the logistical constraints of refrigerated blood.

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