scholarly journals Resuscitation Fluid with Drag Reducing Polymer Enhances Cerebral Microcirculation and Tissue Oxygenation After Traumatic Brain Injury Complicated by Hemorrhagic Shock

2018 ◽  
pp. 39-43 ◽  
Author(s):  
D. E. Bragin ◽  
D. A. Lara ◽  
O. A. Bragina ◽  
M. V. Kameneva ◽  
E. M. Nemoto
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hemorrhagic Shock ◽  
Tissue Oxygenation ◽  
Cerebral Microcirculation ◽  
Resuscitation Fluid ◽  
Drag Reducing Polymer

Abstract WP276: Drag Reducing Polymers Based Resuscitation Fluid Improves Cerebral Microcirculation After Mild Traumatic Brain Injury and Hemorrhagic Shock

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Devon Lara ◽  
Gloria Statom ◽  
Olga A Bragina ◽  
Marina V Kameneva ◽  
Edwin M Nemoto ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Hospital Care ◽  
Microvascular Perfusion ◽  
Arterial Hypotension ◽  
Cerebral Microcirculation ◽  
Neuronal Necrosis ◽  
Resuscitation Fluid

Introduction: Hemorrhagic shock (HS), causing arterial hypotension, often occurs after traumatic brain injury (TBI). Current resuscitation fluids do not ameliorate the impaired cerebral microvascular perfusion leading to hypoxia, neuronal death, increased mortality and poor neurological outcome. Nanomolar concentrations of intravascular blood soluble drag reducing polymers (DRP) were shown to increase tissue perfusion and oxygenation and decrease peripheral vascular resistance by rheological modulation of hemodynamics. We hypothesized that the resuscitation fluid with DRP would improve cerebral microcirculation, oxygenation and neuronal recovery after TBI combined with HS (TBI+HS). Methods: Mild TBI was induced in rats by fluid percussion pulse (1.5 ATA, 50 ms duration) followed by induced by phlebotomy arterial hypotension (40 mmHg). Resuscitation fluid (lactated Ringers, LR) with DRP (DRP/LR) or without (LR) was infused to restore mean arterial pressure (MAP) to 60 mmHg for one hour (pre-hospital care), followed by re-infusion of blood to a MAP of 100 mmHg (hospital care). Using in vivo 2-photon laser scanning microscopy over the parietal cortex we monitored changes in microvascular blood flow, tissue oxygenation (NADH) and neuronal necrosis (i.v. propidium Iodide) for 5 hr after TBI+HS. Doppler cortical flow, rectal and cranial temperatures, arterial pressure, blood gases and electrolytes were monitored. Results: TBI+HS compromised brain microvascular flow leading to tissue hypoxia followed by neuronal necrosis. Resuscitation with DRP/LR compared to LR better improved cerebral microvascular perfusion (82 ± 9.7% vs. 62 ± 9.7%, respectively from pre-TBI baseline, p<0.05, n=7), attenuated capillary microtrombi formation and re-recruited collapsed during HS capillaries. Improved microvascular perfusion increased cortical oxygenation reducing hypoxia (77 ± 8.2% vs. 60 ± 10.5%, by DRP-LR vs. LR, respectively from baseline, p<0.05) and decreased neuronal necrosis (21 ± 7.2% vs. 36 ± 7.3%, respectively as a percentage of total neurons, p<0.05). Conclusions: DRP/LR resuscitation fluid is superior in the restoration of the cerebral microcirculation and neuroprotection following TBI + HS compared to volume expansion with LR.

Shenfu injection improves cerebral microcirculation and reduces brain injury in a porcine model of hemorrhagic shock; SFI reduces brain injury after hemorrhagic shock

2021 ◽  
pp. 1-11
Author(s):  
Junyuan Wu ◽  
Zhiwei Li ◽  
Wei Yuan ◽  
Qiang Zhang ◽  
Yong Liang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Hemorrhagic Shock ◽  
Interleukin 6 ◽  
Aquaporin 4 ◽  
Flow Index ◽  
Sham Operation ◽  
Volume Resuscitation ◽  
Cerebral Microcirculation ◽  
Shenfu Injection ◽  
Tnf Α

BACKGROUND: Shenfu injection (SFI) is a traditional Chinese herbal medicine which has been clinically used for treatment of septic shock and cardiac shock. The aim of this study was to clarify effects of SFI on cerebral microcirculation and brain injury after hemorrhagic shock (HS). METHODS: Twenty-one domestic male Beijing Landrace pigs were randomly divided into three groups: SFI group (SFI, n = 8), saline group (SA, n = 8) or sham operation group (SO, n = 5). In the SFI group, animals were induced to HS by rapid bleeding to a mean arterial pressure of 40 mmHg within 10 minutes and maintained at 40±3 mmHg for 60 minutes. Volume resuscitation (shed blood and crystalloid) and SFI were given after 1 hour of HS. In the SA group, animals received the same dose of saline instead of SFI. In the SO group, the same surgical procedure was performed but without inducing HS and volume resuscitation. The cerebral microvascular flow index (MFI), nitric oxide synthase (NOS) expression, aquaporin-4 expression, interleukin-6, tumor necrosis factor-α (TNF-α) and ultrastructural of microvascular endothelia were measured. RESULTS: Compared with the SA group, SFI significantly improved cerebral MFI after HS. SFI up regulated cerebral endothelial NOS expression, but down regulated interleukin-6, TNF-α, inducible NOS and aquaporin-4 expression compared with the SA group. The cerebral microvascular endothelial injury and interstitial edema in the SFI group were lighter than those in the SA group. CONCLUSIONS: Combined application of SFI with volume resuscitation after HS can improve cerebral microcirculation and reduce brain injury.

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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