Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia

Dhillon, Simerdeep K; Gunn, Alistair J.; Lear, Benjamin A; King, Victoria J; Lear, Christopher A.; Wassink, Guido; Davidson, John B.; Gunn, Alistair J.

doi:10.3389/fped.2022.925951

Cited by 14 publications

(5 citation statements)

References 92 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The decrease in CMRO 2 occurred in the first hours after the HI insult, and during the same time period, CBF was equal to control animals ( 45 ). These findings are in accordance with previously postulated hypothesis of metabolic suppression during the latent phase of injury ( 5 , 46 ). However, no such change in cerebral metabolism was detected in this study as oxygen tension and rSO 2 returned to baseline levels after the HI insult.…”

Section: Discussionsupporting

confidence: 93%

Early changes in cerebral metabolism after perinatal hypoxia-ischemia: a study in normothermic and hypothermic piglets

et al. 2023

View full text Add to dashboard Cite

IntroductionHypoxic ischemic encephalopathy (HIE) after a perinatal insult is a dynamic process that evolves over time. Therapeutic hypothermia (TH) is standard treatment for severe to moderate HIE. There is a lack of evidence on the temporal change and interrelation of the underlying mechanisms that constitute HIE under normal and hypothermic conditions. We aimed to describe early changes in intracerebral metabolism after a hypoxic-ischemic insult in piglets treated with and without TH and in controls.MethodsThree devices were installed into the left hemisphere of 24 piglets: a probe measuring intracranial pressure, a probe measuring blood flow and oxygen tension, and a microdialysis catheter measuring lactate, glucose, glycerol, and pyruvate. After a standardized hypoxic ischemic insult, the piglets were randomized to either TH or normothermia.ResultsGlycerol, a marker of cell lysis, increased immediately after the insult in both groups. There was a secondary increase in glycerol in normothermic piglets but not in piglets treated with TH. Intracerebral pressure, blood flow, oxygen tension, and extracellular lactate remained stable during the secondary increase in glycerol.ConclusionThis exploratory study depicted the development of the pathophysiological mechanisms in the hours following a perinatal hypoxic-ischemic insult with and without TH and controls.

show abstract

Section: Discussionsupporting

confidence: 93%

Early changes in cerebral metabolism after perinatal hypoxia-ischemia: a study in normothermic and hypothermic piglets

et al. 2023

View full text Add to dashboard Cite

show abstract

“…The current single-cell transcriptomic sequencing also found that the two have similar phenotypes ( 89 ). Activated microglia/macrophages have been found to produce a variety of mediators, including iNOS ( 90 ), inflammatory cytokines (such as TNF-α, IL-1β, TGF-β, IL-10) ( 86 ), nerve growth and trophic factors (such as IGF-1, bFGF, PDGF, BDNF) ( 91 ).…”

Section: Mechanisms Of Microglia/macrophages In Ismentioning

confidence: 99%

The mechanism of microglia-mediated immune inflammation in ischemic stroke and the role of natural botanical components in regulating microglia: A review

et al. 2023

View full text Add to dashboard Cite

Ischemic stroke (IS) is one of the most fatal diseases. Neuroimmunity, inflammation, and oxidative stress play important roles in various complex mechanisms of IS. In particular, the early proinflammatory response resulting from the overactivation of resident microglia and the infiltration of circulating monocytes and macrophages in the brain after cerebral ischemia leads to secondary brain injury. Microglia are innate immune cells in the brain that constantly monitor the brain microenvironment under normal conditions. Once ischemia occurs, microglia are activated to produce dual effects of neurotoxicity and neuroprotection, and the balance of the two effects determines the fate of damaged neurons. The activation of microglia is defined as the classical activation (M1 type) or alternative activation (M2 type). M1 type microglia secrete pro-inflammatory cytokines and neurotoxic mediators to exacerbate neuronal damage, while M2 type microglia promote a repairing anti-inflammatory response. Fine regulation of M1/M2 microglial activation to minimize damage and maximize protection has important therapeutic value. This review focuses on the interaction between M1/M2 microglia and other immune cells involved in the regulation of IS phenotypic characteristics, and the mechanism of natural plant components regulating microglia after IS, providing novel candidate drugs for regulating microglial balance and IS drug development.

show abstract

“…Its onset and progression depend on the extent and severity of the injury. The more severe the injury, the earlier the onset of the secondary phase [29]. Although the exact mechanism of the secondary energy failure remains unknown, necrosis and reperfusion injury in the neonatal brain following primary energy failure are considered key factors.…”

Section: Pathophysiology and Neural Cell Deathmentioning

confidence: 99%

Advances in Therapies to Treat Neonatal Hypoxic-Ischemic Encephalopathy

Ranjan,

Gulati

2023

JCM

View full text Add to dashboard Cite

Neonatal hypoxic-ischemic encephalopathy (HIE) is a condition that results in brain damage in newborns due to insufficient blood and oxygen supply during or after birth. HIE is a major cause of neurological disability and mortality in newborns, with over one million neonatal deaths occurring annually worldwide. The severity of brain injury and the outcome of HIE depend on several factors, including the cause of oxygen deprivation, brain maturity, regional blood flow, and maternal health conditions. HIE is classified into mild, moderate, and severe categories based on the extent of brain damage and resulting neurological issues. The pathophysiology of HIE involves different phases, including the primary phase, latent phase, secondary phase, and tertiary phase. The primary and secondary phases are characterized by episodes of energy and cell metabolism failures, increased cytotoxicity and apoptosis, and activated microglia and inflammation in the brain. A tertiary phase occurs if the brain injury persists, characterized by reduced neural plasticity and neuronal loss. Understanding the cellular and molecular aspects of the different phases of HIE is crucial for developing new interventions and therapeutics. This review aims to discuss the pathophysiology of HIE, therapeutic hypothermia (TH), the only approved therapy for HIE, ongoing developments of adjuvants for TH, and potential future drugs for HIE.

show abstract

Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia

Cited by 14 publications

References 92 publications

Early changes in cerebral metabolism after perinatal hypoxia-ischemia: a study in normothermic and hypothermic piglets

Early changes in cerebral metabolism after perinatal hypoxia-ischemia: a study in normothermic and hypothermic piglets

The mechanism of microglia-mediated immune inflammation in ischemic stroke and the role of natural botanical components in regulating microglia: A review

Advances in Therapies to Treat Neonatal Hypoxic-Ischemic Encephalopathy

Contact Info

Product

Resources

About