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.

scholarly journals C1q/CTRP1 exerts neuroprotective effects in TBI rats by regulating inflammation and autophagy

2020 ◽  
Author(s):  
Ming Pei ◽  
Chaoqun Wang ◽  
Zhengdong Li ◽  
Jianhua Zhang ◽  
Ping Huang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Inflammatory Factors ◽  
Vehicle Group ◽  
Secondary Brain Injury ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia Reperfusion Injury

AbstractObjectiveC1q/CTRP1 is a newly discovered adiponectin protein, which is highly expressed in adipose and heart tissues. Recent studies have revealed that C1q/CTRP1 can regulate metabolism and inhibit inflammation. CTRP1 is also expressed in brain tissues and vascular cells of human and rat, and research on cerebral hemorrhage and cerebral ischemia-reperfusion injury demonstrates that the CTRP family can attenuate secondary brain injury and exert neuroprotective effects. Thus, this study was designed to explore the role of CTRP1 in traumatic brain injury (TBI) and the underlying mechanism.Main methodsRats were assigned into rCTRP1 group, vehicle group, and sham group. Modified Feeney’s method was used to establish a closed traumatic brain injury model. Morris water maze was used for directional navigation, reverse searching and space exploration tests in rats. In addition, Golgi-Cox staining was utilized to visualize neurons, dendrites and dendritic spines. ELISA was conducted to detect the levels of inflammatory factors (IL-6 and TNF-α). Finally, Western blot was adopted to detect the relative expression of p-mTOR and autophagy-related proteins (Beclin-1 and LC3-II).ResultsCTRP1 improved the behavioral and histopathological outcomes, inhibited the inflammatory response, activated mTOR and decreased autophagy-associated protein synthesis in TBI rats.ConclusionCTRP1 exerts neuroprotective effects in TBI rats by regulating inflammation and autophagy and has potential therapeutic properties after TBI.

scholarly journals Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

2010 ◽  
Vol 31 (1) ◽  
pp. 17-35 ◽  
Author(s):  
Martin Lauritzen ◽  
Jens Peter Dreier ◽  
Martin Fabricius ◽  
Jed A Hartings ◽  
Rudolf Graf ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Disorders ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Neuronal Damage ◽  
Ion Homeostasis ◽  
Large Body ◽  
Treatment Strategies ◽  
Pathophysiological Mechanism

Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. The implications of these findings are widespread and suggest that intrinsic brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute brain disorders in the intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves.

HEMORRHAGIC SHOCK AND RESUSCITATION IN ORGAN DONORS INCREASES ISCHEMIA REPERFUSION INJURY OF LUNG GRAFTS.

Shock ◽  
2004 ◽  
Vol 21 (Supplement) ◽  
pp. 89
Author(s):  
G Preissler ◽  
U Ebersberger ◽  
I Huff ◽  
M Eichhorn ◽  
K Memer ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Organ Donors

scholarly journals A Hypothesis: Hydrogen Sulfide Might Be Neuroprotective against Subarachnoid Hemorrhage Induced Brain Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Yong-Peng Yu ◽  
Xiang-Lin Chi ◽  
Li-Jun Liu
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Leukocyte Adhesion ◽  
Ischemia Reperfusion ◽  
The Brain

Gases such as nitric oxide (NO) and carbon monoxide (CO) play important roles both in normal physiology and in disease. Recent studies have shown that hydrogen sulfide (H2S) protects neurons against oxidative stress and ischemia-reperfusion injury and attenuates lipopolysaccharides (LPS) induced neuroinflammation in microglia, exhibiting anti-inflammatory and antiapoptotic activities. The gas H2S is emerging as a novel regulator of important physiologic functions such as arterial diameter, blood flow, and leukocyte adhesion. It has been known that multiple factors, including oxidative stress, free radicals, and neuronal nitric oxide synthesis as well as abnormal inflammatory responses, are involved in the mechanism underlying the brain injury after subarachnoid hemorrhage (SAH). Based on the multiple physiologic functions of H2S, we speculate that it might be a promising, effective, and specific therapy for brain injury after SAH.

scholarly journals Ferroptosis: A Novel Therapeutic Target for Ischemia-Reperfusion Injury

2021 ◽  
Vol 9 ◽  
Author(s):  
Yunqing Chen ◽  
Hongyan Fan ◽  
Shijun Wang ◽  
Guanmin Tang ◽  
Changlin Zhai ◽  
...  
Keyword(s):  
Cell Death ◽  
Therapeutic Target ◽  
Ischemia Reperfusion Injury ◽  
Close Association ◽  
Ischemia Reperfusion ◽  
Treatment Strategies ◽  
Kidney Injury ◽  
Organ Damage ◽  
Current Treatment ◽  
Current Status

Ischemia-reperfusion (I/R) injury is a major cause of cell death and organ damage in numerous pathologies, including myocardial infarction, stroke, and acute kidney injury. Current treatment methods for I/R injury are limited. Ferroptosis, which is a newly uncovered type of regulated cell death characterized by iron overload and lipid peroxidation accumulation, has been investigated in various diseases. There is increasing evidence of a close association between ferroptosis and I/R injury, with ferroptosis frequently identified as a new therapeutic target for the management of I/R injury. This review summarizes the current status of ferroptosis and discusses its relationship with I/R injury, as well as potential treatment strategies targeting it.

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.

Traumatic Brain Injury

2008 ◽  
Author(s):  
Vani Rao
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Major Depression ◽  
Psychiatric Disorders ◽  
Financial Burden ◽  
Treatment Strategies ◽  
Chronic Alcoholism ◽  
The United States ◽  
Psychiatric Disturbances ◽  
Psychotic Features

Traumatic brain injury (TBI) is a significant cause of disability in the United States, with an incidence of about 1.5 million cases per year (National Institutes of Health Consensus Development Panel, 1999). It is associated with both neurologic and psychiatric consequences. Although the neurologic problems usually stabilize with time, the psychiatric disorders often continue to remit and relapse. Factors associated with the development of psychiatric disorders include older age, arteriosclerosis, and chronic alcoholism, all of which interfere with the reparative process within the central nervous system. Other contributors to psychiatric disability include a pre-TBI history of psychiatric illness, illicit drug abuse, and lack of social support. Because post-TBI psychiatric disturbances interfere with rehabilitation and cause emotional and financial burden for patients and caregivers, early diagnosis and treatment are important. Post-TBI psychiatric disturbances are best classified according to their clinical presentation. These disturbances are discussed below and their pharmacologic and nonpharmacologic treatment strategies are recommended. The mood disturbances most commonly associated with TBI are major depression, mania, anxiety, and apathy. Major depression is seen in about 25% of people with TBI. Symptoms of major depression include persistent sadness; guilt; feelings of worthlessness; hopelessness; suicidal thoughts; anhedonia; and changes in patterns of sleep, appetite, and energy. Sometimes these symptoms may be associated with psychotic features such as delusions and hallucinations. It is important to remember that changes in sleep, appetite, or energy are not specific to the syndrome of major depression and may be due to the brain injury itself, or to the noise, stimulation, or deconditioning associated with hospitalization. If due to the latter conditions, gradual improvement occurs with time in most patients. Sadness in excess of the severity of injury and poor participation in rehabilitation are strong indicators of the presence of major depression. The presence of poor social functioning pre-TBI and left dorsolateral frontal and/or left basal ganglia lesion have been associated with an increased probability of developing major depression following brain injury ( Jorge et al., 1993a; Jorge et al., 2004). Major depression should be differentiated from demoralization, primary apathy syndrome, and pathologic crying.

scholarly journals Hyponatremia in the Neurologically Ill Patient: A Review

2020 ◽  
Vol 10 (3) ◽  
pp. 208-216
Author(s):  
David P. Lerner ◽  
Starane A. Shepherd ◽  
Ayush Batra
Keyword(s):  
Traumatic Brain Injury ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Early Diagnosis ◽  
Neurological Disorders ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Treatment Strategies ◽  
Diagnosis And Treatment ◽  
Systemic Complications ◽  
Acute Presentation

Hyponatremia is a well-known disorder commonly faced by clinicians managing neurologically ill patients. Neurological disorders are often associated with hyponatremia during their acute presentation and can be associated with specific neurologic etiologies and symptoms. Patients may present with hyponatremia with traumatic brain injury, develop hyponatremia subacutely following aneurysmal subarachnoid hemorrhage, or may manifest with seizures due to hyponatremia itself. Clinicians caring for the neurologically ill patient should be well versed in identifying these early signs, symptoms, and etiologies of hyponatremia. Early diagnosis and treatment can potentially avoid neurologic and systemic complications in these patients and improve outcomes. This review focuses on the causes and findings of hyponatremia in the neurologically ill patient and discusses the pathophysiology, diagnoses, and treatment strategies for commonly encountered etiologies.

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