scholarly journals Neuroprotection Against Hypoxic/Ischemic Injury: δ-Opioid Receptors and BDNF-TrkB Pathway

2018 ◽  
Vol 47 (1) ◽  
pp. 302-315 ◽  
Author(s):  
Shiying Sheng ◽  
Jingzhong Huang ◽  
Yi Ren ◽  
Feng Zhi ◽  
Xuansong Tian ◽  
...  
Keyword(s):  
Opioid Receptors ◽  
Ischemic Injury ◽  
Mammalian Brain ◽  
Ionic Homeostasis ◽  
Ischemic Brain ◽  
Neuronal Transmission ◽  
The Brain ◽  
Excitatory Transmitter ◽  
Hypoxic Ischemic Injury ◽  
Ischemic Stress

The delta-opioid receptor (DOR) is one of three classic opioid receptors in the opioid system. It was traditionally thought to be primarily involved in modulating the transmission of messages along pain signaling pathway. Although there were scattered studies on its other neural functions, inconsistent results and contradicting conclusions were found in past literatures, especially in terms of DOR’s role in a hypoxic/ischemic brain. Taking inspiration from the finding that the turtle brain exhibits a higher DOR density and greater tolerance to hypoxic/ischemic insult than the mammalian brain, we clarified DOR’s specific role in the brain against hypoxic/ischemic injury and reconciled previous controversies in this aspect. Our serial studies have strongly demonstrated that DOR is a unique neuroprotector against hypoxic/ischemic injury in the brain, which has been well confirmed in current research. Moreover, mechanistic studies have shown that during acute phases of hypoxic/ischemic stress, DOR protects the neurons mainly by the stabilization of ionic homeostasis, inhibition of excitatory transmitter release, and attenuation of disrupted neuronal transmission. During prolonged hypoxia/ischemia, however, DOR neuroprotection involves a variety of signaling pathways. More recently, our data suggest that DOR may display its neuroprotective role via the BDNF-TrkB pathway. This review concisely summarizes the progress in this field.

scholarly journals NEUROSONOGRAPHIC STUDY OF CHILDREN WITH HYPOXIC-ISCHEMIC BRAIN IJURY

2020 ◽  
pp. 7-11
Author(s):  
Volotko L. O.
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Brain Injury ◽  
Brain Tissue ◽  
Ischemic Injury ◽  
Ischemic Brain ◽  
Destructive Processes ◽  
The Brain ◽  
Hypoxic Ischemic Injury

The study is aimed at neurosonographic characteristics of brain injury in newborn patients with perinatal hypoxic-ischemic injury of central nervous system, complicated with inflectional process (meningitis, ventriculitis). It is settled that brain immaturity, hydrocephalic syndrome, ischemia of the brain tissue and intraventricular hemorrhages are found 2 times more often in infants with perinatal hypoxic-ischemic injury of central nervous system, complicated with inflectional process. This fact generally characterizes disorders of the hemato-encephalic barrier and the development of destructive processes in the tissue of the brain.

scholarly journals Pretreatment with Monosialoganglioside GM1 Protects the Brain of Fetal Sheep against Hypoxic-Ischemic Injury without Causing Systemic Compromise

1993 ◽  
Vol 34 (1) ◽  
pp. 18-22 ◽  
Author(s):  
William K M Tan ◽  
Chris E Williams ◽  
Alistair J Gunn ◽  
E Carina Mallard ◽  
Peter D Gluckman
Keyword(s):  
Ischemic Injury ◽  
Fetal Sheep ◽  
The Brain ◽  
Hypoxic Ischemic Injury

scholarly journals Fetal stress-mediated hypomethylation increases the brain susceptibility to hypoxic–ischemic injury in neonatal rats

2016 ◽  
Vol 275 ◽  
pp. 1-10 ◽  
Author(s):  
Yong Li ◽  
Qingyi Ma ◽  
Shina Halavi ◽  
Katherine Concepcion ◽  
Richard E. Hartman ◽  
...  
Keyword(s):  
Ischemic Injury ◽  
Neonatal Rats ◽  
The Brain ◽  
Hypoxic Ischemic Injury

scholarly journals Calcium Accumulation during the Evolution of Hypoxic—Ischemic Brain Damage in the Immature Rat

1988 ◽  
Vol 8 (6) ◽  
pp. 834-842 ◽  
Author(s):  
Dagmar T. Stein ◽  
Robert C. Vannucci
Keyword(s):  
Brain Damage ◽  
Cerebral Hemisphere ◽  
Ischemic Injury ◽  
Calcium Flux ◽  
Variable Degree ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Calcium Accumulation ◽  
Hypoxia Ischemia ◽  
Hypoxic Ischemic Injury

An excessive accumulation of calcium in neuronal and other tissues has been postulated to represent a “final common pathway” for cell death arising from hypoxia-ischemia. To clarify the role of altered calcium flux into and distribution within the perinatal brain undergoing hypoxic-ischemic injury, 7-day postnatal rats underwent unilateral common carotid artery ligation followed by 3 h of hypoxia with 8% oxygen. This insult is known to produce brain damage confined to the cerebral hemisphere ipsilateral to the arterial occlusion in >90% of the animals. Either before or after hypoxia-ischemia, the animals received a subcutaneous injection of [45Ca]Cl2, and their brains were subjected to 45Ca autoradiography at 0–1, 5, 24, and 72 h, 7 or 15 days thereafter. During hypoxia-ischemia, calcium flux into the ipsilateral cerebral hemisphere was prominent in 13 of 14 rat pups, especially in neocortex, hippocampus, striatum, and thalamus. Calcium accumulation also occurred to a variable degree (6 of 14 animals) in the contralateral cerebral hemisphere. During recovery, radioactivity in the contralateral cerebral hemisphere was no longer apparent, whereas in the ipsilateral hemisphere, the extent of calcium accumulation was mild in four of six at 1 h, moderate in three of six at 5 h, moderate to intense in six of seven and six of seven at 24 and 72 h, respectively, and intense in three of three and two of two animals at 7 and 15 days, respectively. As during hypoxia-ischemia, the distribution of the radioactivity was most prominent in those structures that are known to be vulnerable to hypoxic-ischemic injury. Thus, hypoxia-ischemia is associated with enhanced calcium uptake into the immature brain, which does not dissipate but rather progressively accumulates for up to 15 days of recovery. The findings implicate a disruption of intracellular calcium homeostasis as a major factor in the evolution of perinatal hypoxic-ischemic brain damage.

Abstract 13824: Computerized Tomography vs Ultrasound Imaging for Detecting Hypoxic-Ischemic Brain Injury

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Benjamin Karfunkle ◽  
Pavitra Kotini-shah ◽  
Richard Gordon ◽  
Jing Li ◽  
Misha Granado ◽  
...  
Keyword(s):  
Brain Injury ◽  
Hospital Discharge ◽  
Computerized Tomography ◽  
Point Of Care ◽  
Ischemic Injury ◽  
Ct Head ◽  
Ct Brain ◽  
Initial Imaging ◽  
The Brain ◽  
Hypoxic Ischemic Injury

Introduction: After an out-of-hospital cardiac arrest (OHCA), the resulting hypoxic-ischemic injury (HII) to the brain remains the main cause of mortality. Standardized approaches for measuring the extent of injury and monitoring of changes are lacking and continue to be a critical barrier to progress in improving neurological survival. Objective: We sought to characterize the prevalence of HII detected on computerized tomography of the brain and its correlation to point-of-care optic nerve sheath diameter (ONSD) measurements as an alternative modality for detecting brain injury. Methods: Adult OHCA patients at an urban academic ED were included in this study on a convenience sample basis from 2018-2019. The patients were grouped by findings of hypoxic-ischemic injury (HII) on both initial and subsequent CT brain imaging performed after ROSC in respective groups. CT Brain findings were compared to ONSD measurements as performed with point-of-care ultrasound by fellowship-trained emergency physicians within one hour of hospital arrival and at 6 hours, after return of spontaneous circulation (ROSC) and to cerebral performance category (CPC) at hospital discharge. Results: 76 patients enrolled in the study had a median age was 59, 49% were female, and 37% survived to hospital discharge. 58 patients had CT head performed, 40 had ONSD measured within one hour, and 27 patients had both. Of that 27, 9 (33%) had evidence of HII on initial imaging and 15 (55%) had evidence of HII on subsequent imaging for a total of 20 unique patients. The average ONSD within 1 hour of ROSC for those with no HII on any imaging was 0.59 cm, and for those without HII on initial imaging but with HII on subsequent imaging was 0.67 cm, and this difference was statistically significant (p< 0.05). Of the 20 patients with HI, 14 (70%) patients died and 6 (30%) survived with a CPC of 4. The average time to first CT head was 4 hours and 45 mins and the average time to subsequent imaging was 97 hours and 45 mins. Conclusion: After an OHCA, early time point ONSD measurements can potentially indicate brain injury within 1 hour of ROSC even in those without initial evidence of HII on CT imaging.

scholarly journals Immunomodulation with Human Umbilical Cord Blood Stem Cells Ameliorates Ischemic Brain Injury – A Brain Transcriptome Profiling Analysis

2019 ◽  
Vol 28 (7) ◽  
pp. 864-873 ◽  
Author(s):  
Maple L. Shiao ◽  
Ce Yuan ◽  
Andrew T. Crane ◽  
Joseph P. Voth ◽  
Mario Juliano ◽  
...  
Keyword(s):  
Stem Cells ◽  
Brain Injury ◽  
Umbilical Cord Blood ◽  
Ischemic Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Brain Transcriptome ◽  
Blood Stem Cells ◽  
Cord Blood Stem Cells ◽  
The Brain

Our group previously demonstrated that administration of a CD34-negative fraction of human non- hematopoietic umbilical cord blood stem cells (UCBSC) 48 h after ischemic injury could reduce infarct volume by 50% as well as significantly ameliorate neurological deficits. In the present study, we explored possible mechanisms of action using next generation RNA sequencing to analyze the brain transcriptome profiles in rats with ischemic brain injury following UCBSC therapy. Two days after ischemic injury, rats were treated with UCBSC. Five days after administration, total brain mRNA was then extracted for RNAseq analysis using Illumina Hiseq 2000. We found 275 genes that were significantly differentially expressed after ischemic injury compared with control brains. Following UCBSC treatment, 220 of the 275 differentially expressed genes returned to normal levels. Detailed analysis of these altered transcripts revealed that the vast majority were associated with activation of the immune system following cerebral ischemia which were normalized following UCBSC therapy. Major alterations in gene expression profiles after ischemia include blood-brain-barrier breakdown, cytokine production, and immune cell infiltration. These results suggest that UCBSC protect the brain following ischemic injury by down regulating the aberrant activation of innate and adaptive immune responses.

scholarly journals Function of neural stem cells in ischemic brain repair processes

2016 ◽  
Vol 36 (12) ◽  
pp. 2034-2043 ◽  
Author(s):  
Ruilan Zhang ◽  
Zhenggang Zhang ◽  
Michael Chopp
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Subventricular Zone ◽  
Ischemic Injury ◽  
Neurological Function ◽  
Repair Capacity ◽  
Modest Improvement ◽  
Ischemic Brain ◽  
Injured Brain ◽  
Hypoxic Ischemic Injury

Hypoxic/ischemic injury is the single most important cause of disabilities in infants, while stroke remains a leading cause of morbidity in children and adults around the world. The injured brain has limited repair capacity, and thereby only modest improvement of neurological function is evident post injury. In rodents, embryonic neural stem cells in the ventricular zone generate cortical neurons, and adult neural stem cells in the ventricular–subventricular zone of the lateral ventricle produce new neurons through animal life. In addition to generation of new neurons, neural stem cells contribute to oligodendrogenesis. Neurogenesis and oligodendrogenesis are essential for repair of injured brain. Much progress has been made in preclinical studies on elucidating the cellular and molecular mechanisms that control and coordinate neurogenesis and oligodendrogenesis in perinatal hypoxic/ischemic injury and the adult ischemic brain. This article will review these findings with a focus on the ventricular–subventricular zone neurogenic niche and discuss potential applications to facilitate endogenous neurogenesis and thereby to improve neurological function post perinatal hypoxic/ischemic injury and stroke.

Sign in / Sign up

Export Citation Format

Share Document