Prolonged Severe Hemorrhagic Shock and Resuscitation in Rats Does Not Cause Subtle Brain Damage

Carrillo, Peter; Takasu, Akira; Šafář, Peter; Tisherman, Samuel A.; Stezoski, S. William; Stolz, G; Dixon, C. Edward; Radovsky, Ann

doi:10.1097/00005373-199808000-00007

Cited by 47 publications

(31 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, by 21 days, significant CA3 cell death was not evident in either insult. HS alone did not produce appreciable CA1 or CA3 death as assessed by FJC or H&E cell counts, consistent with our prior work (Carrillo et al, 1998;Dennis et al, 2009). Adding an HS insult with a MAP of *35-45 mm Hg for 90 min after CCI exacerbated only CA1 cell death (Dennis et al, 2009).…”

supporting

confidence: 86%

Severe Brief Pressure-Controlled Hemorrhagic Shock after Traumatic Brain Injury Exacerbates Functional Deficits and Long-Term Neuropathological Damage in Mice

Hemerka

Dixon

et al. 2012

Journal of Neurotrauma

Self Cite

View full text Add to dashboard Cite

Hypotension after traumatic brain injury (TBI) worsens outcome. We published the first report of TBI plus hemorrhagic shock (HS) in mice using a volume-controlled approach and noted increased neuronal death. To rigorously control blood pressure during HS, a pressure-controlled HS model is required. Our hypothesis was that a brief, severe period of pressure-controlled HS after TBI in mice will exacerbate functional deficits and neuropathology versus TBI or HS alone. C57BL6 male mice were randomized into four groups (n = 10/group): sham, HS, controlled cortical impact (CCI), and CCI + HS. We used a pressure-controlled shock phase (mean arterial pressure [MAP] = 25-27 mm Hg for 35 min) and its treatment after mild to moderate CCI including, a 90 min pre-hospital phase, during which lactated Ringer's solution was given to maintain MAP > 70 mm Hg, and a hospital phase, when the shed blood was re-infused. On days 14-20, the mice were evaluated in the Morris water maze (MWM, hidden platform paradigm). On day 21, the lesion and hemispheric volumes were quantified. Neuropathology and hippocampal neuron counts (hematoxylin and eosin [H&E], Fluoro-Jade B, and NeuN) were evaluated in the mice (n = 60) at 24 h, 7 days, or 21 days (n = 5/group/time point). HS reduced MAP during the shock phase in the HS and CCI + HS groups ( p < 0.05). Fluid requirements during the pre-hospital phase were greatest in the CCI + HS group ( p < 0.05), and were increased in HS versus sham and CCI animals ( p < 0.05). MWM latency was increased on days 14 and 15 after CCI + HS ( p < 0.05). Swim speed and visible platform latency were impaired in the CCI + HS group ( p < 0.05). CCI + HS animals had increased contusion volume versus the CCI group ( p < 0.05). Hemispheric volume loss was increased 33.3% in the CCI + HS versus CCI group ( p < 0.05). CA1 cell loss was seen in CCI + HS and CCI animals at 24 h and 7 days ( p < 0.05). CA3 cell loss was seen after CCI + HS ( p < 0.05 at 24 h and 7 days). CA1 cell loss at 21 days was seen only in CCI + HS animals ( p < 0.05). Brief, severe, pressure-controlled HS after CCI produces robust functional deficits and exacerbates neuropathology versus CCI or HS alone.

show abstract

supporting

confidence: 86%

Severe Brief Pressure-Controlled Hemorrhagic Shock after Traumatic Brain Injury Exacerbates Functional Deficits and Long-Term Neuropathological Damage in Mice

Hemerka

Dixon

et al. 2012

Journal of Neurotrauma

Self Cite

View full text Add to dashboard Cite

show abstract

“…However, it is important to note that all animals were subjected to the same catheterizations. This is in concert with results of another study reporting no persistent limb ischemia or functional deficits after femoral vessel cannulation and ligation in rats assessed with an identical battery of motor tests (Carrillo et al, 1998).…”

Section: Discussionsupporting

confidence: 87%

“…A modified Morris water maze (MWM) task was used to evaluate spatial learning and memory (Morris, 1984;Carrillo et al, 1998). The maze used a 1.8 m diameter and 60 cm high pool filled with non-opaque water (25-27°C) to a depth of 28 cm and a clear Plexiglas stand 10 cm in diameter.…”

Section: Methodsmentioning

confidence: 99%

Prolonged deep hypothermic circulatory arrest in rats can be achieved without cognitive deficits

et al. 2007

Self Cite

View full text Add to dashboard Cite

“…Previous studies from our laboratory showed that with femoral artery cannulation and shock at MAP ϭ 20 to 25 mmHg for 30 min, survival was nearly 100%, even in animals receiving no resuscitation (shocked, nonresuscitated, controls; unpublished data). Lethal rat hemorrhagic models from different investigators have shown that MAP was lower and the shock time was longer using femoral cannulation than with carotid cannulation [2][3][4][5]. In one study, no functional or histological brain damage was noted in rats cannulated through the femoral artery and bled to a MAP of 40 mmHg for 60 min, or a MAP of 30 mmHg for 45 min [5].…”

Section: Discussionmentioning

confidence: 99%

Hemorrhagic Shock in the Rat: Comparison of Carotid and Femoral Cannulation

Yang

Tan

Kenney

et al. 2008

Journal of Surgical Research

View full text Add to dashboard Cite

Prolonged Severe Hemorrhagic Shock and Resuscitation in Rats Does Not Cause Subtle Brain Damage

Cited by 47 publications

References 26 publications

Severe Brief Pressure-Controlled Hemorrhagic Shock after Traumatic Brain Injury Exacerbates Functional Deficits and Long-Term Neuropathological Damage in Mice

Severe Brief Pressure-Controlled Hemorrhagic Shock after Traumatic Brain Injury Exacerbates Functional Deficits and Long-Term Neuropathological Damage in Mice

Prolonged deep hypothermic circulatory arrest in rats can be achieved without cognitive deficits

Hemorrhagic Shock in the Rat: Comparison of Carotid and Femoral Cannulation

Contact Info

Product

Resources

About