Neuroprotective gases – Fantasy or reality for clinical use?

Deng, Jiao; Lei, Chong; Yu, Chen; Fang, Zongping; Yang, Qianzi; Zhang, Haopeng; Cai, Min; Shi, Likai; Dong, Hailong; Xiong, Lize

doi:10.1016/j.pneurobio.2014.01.001

Cited by 108 publications

(86 citation statements)

References 385 publications

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“…In line with these findings, others have demonstrated that exposure to isoflurane at or near the time of experimental TBI protects against apoptosis, excitotoxicity, inflammation, and vascular damage compared to several other anesthetics [51,75]. Modulation of secondary injury mechanisms by volatile anesthetics can yield long-term consequences in terms of histological and neurological outcomes after TBI [52], with some investigators even advocating for their potential application as neuroprotective agents in the clinical setting [76]. Our findings warrant caution and careful consideration of future study designs, particularly for those involving mTBIs where certain anesthetics may mask subtle adverse events that give rise to long-term changes in behaviors.…”

Section: Discussionmentioning

confidence: 90%

Long-Term Anesthetic-Dependent Hypoactivity after Repetitive Mild Traumatic Brain Injuries in Adolescent Mice

et al. 2016

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Recent evidence supports the hypothesis that repetitive mild traumatic brain injuries (rmTBIs) culminate in neurological impairments and chronic neurodegeneration, which have wide-ranging implications for patient management and return-to-play decisions for athletes. Adolescents show a high prevalence of sports-related head injuries and may be particularly vulnerable to rmTBIs due to ongoing brain maturation. However, it remains unclear whether rmTBIs, below the threshold for acute neuronal injury or symptomology, influence long-term outcomes. To address this issue, we first defined a very mild injury in adolescent mice (postnatal day 35) as evidenced by an increase in Iba-1- labeled microglia in white matter in the acutely injured brain, in the absence of indices of cell death, axonal injury, and vasogenic edema. Using this level of injury severity and Avertin (2,2,2-tribromoethanol) as the anesthetic, we compared mice subjected to either a single mTBI or 2 rmTBIs, each separated by 48 h. Neurobehavioral assessments were conducted at 1 week and at 1 and 3 months postimpact. Mice subjected to rmTBIs showed transient anxiety and persistent and pronounced hypoactivity compared to sham control mice, alongside normal sensorimotor, cognitive, social, and emotional function. As isoflurane is more commonly used than Avertin in animal models of TBI, we next examined long-term outcomes after rmTBIs in mice that were anesthetized with this agent. However, there was no evidence of abnormal behaviors even with the addition of a third rmTBI. To determine whether isoflurane may be neuroprotective, we compared the acute pathology after a single mTBI in mice anesthetized with either Avertin or isoflurane. Pathological findings were more pronounced in the group exposed to Avertin compared to the isoflurane group. These collective findings reveal distinct behavioral phenotypes (transient anxiety and prolonged hypoactivity) that emerge in response to rmTBIs. Our findings further suggest that selected anesthetics may confer early neuroprotection after rmTBIs, and as such mask long-term abnormal phenotypes that may otherwise emerge as a consequence of acute pathogenesis.

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Section: Discussionmentioning

confidence: 90%

Long-Term Anesthetic-Dependent Hypoactivity after Repetitive Mild Traumatic Brain Injuries in Adolescent Mice

et al. 2016

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“…In the central nervous system, hydrogen sulfide is involved in physiological processes, i.e. neuroprotection [51,[94][95][96] and neurotransmission in various models [97][98][99]. Studies using, H 2 S inhalation demonstrated a neuroprotective action in a mouse model of Parkinson's disease [100].…”

Section: H 2 S As a Signaling Molecule In The Nervous Systemmentioning

confidence: 99%

“…Hydrogen sulfide may be involved in protecting neurons from apoptosis and degeneration [101]. Moreover, the mechanisms underlying the neuroprotective effects of H 2 S appear to include also anti-inflammation action and upregulation antioxidative enzymes [96]. Results of Lu et al [102] indicate that hydrogen sulfide regulates intracellular pH in microglial cells and it limits the damage of activated microglia at the site of injury providing a neuroprotective function [101].…”

Section: H 2 S As a Signaling Molecule In The Nervous Systemmentioning

confidence: 99%

Hydrogen sulfide in signaling pathways

Olas

2015

Clinica Chimica Acta

161

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“…İskemik inme modellerinde, kannabinoid reseptör agonistleri, opioid reseptör agonistleri, vanilloid 1 agonistleri, nörotensin analogları, tiroksin türevleri, dopamin reseptör aktivatörleri, helyum, adenozin ve adenin nükleotidleri hipotermiyi indükler 72,73 ancak metabolizma üzerine başkaca etkileri olduğundan koruyucu etkiyi sadece hipotermiyle ilişkilendirmek mümkün olmamaktadır. Bu ajanların farmakodinamisi üzerinde daha fazla çalışmaya ihtiyaç vardır.…”

Section: Farmakolojik Yöntemlerunclassified

İnme ve Terapötik Hipotermi

Kuşçu¹,

Özcengiz²

2016

Arşiv Kaynak Tarama Dergisi

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Stroke is significant cause of morbidity and mortality caused by disruption of blood flow. Neural injury occurs with two stage; while primary neural injury occurs with disruption of blood flow, after days and hours with metabolic processes secondary injury develops in tissues which is non injured in the first stage. Therefore it is important to prevent and treat the secondary injury as much as preventing and treating the primary neural injury. In this article developing pathophysiological changes after stroke, mechanisms of therapeutic hypothermia, application methods, the factors that determine the effectiveness, side effects and complications were reviewed. Key words: Stroke, therapeutic hypothermia, neural injury. ÖZETİnme, beyin kan akımının bozulmasıyla meydana gelen önemli bir morbidite ve mortalite nedenidir. İnmede nöral hasar iki aşamada oluşur; akımın bozulmasıyla primer nöral hasar meydana gelirken, saatler ya da günler sonra gelişen metabolik süreçlerle de ilk aşamada zedelenmeyen dokuda sekonder nöral hasar oluşur. Dolayısıyla primer hasarın önlenmesi ve tedavisi kadar, sekonder nöral hasarın önlenmesi ve tedavisi de önemlidir. Bu derlemede, inme sonrası gelişen patofizyolojik değişiklikler ile terapötik hipoterminin etki mekanizmaları, uygulama yöntemleri, etkinliğini belirleyen faktörler, yan etkileri ve komplikasyonları incelenmiştir. Anahtar kelimeler: İnme, terapötik hipotermi, nöral hasar.

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Neuroprotective gases – Fantasy or reality for clinical use?

Cited by 108 publications

References 385 publications

Long-Term Anesthetic-Dependent Hypoactivity after Repetitive Mild Traumatic Brain Injuries in Adolescent Mice

Long-Term Anesthetic-Dependent Hypoactivity after Repetitive Mild Traumatic Brain Injuries in Adolescent Mice

Hydrogen sulfide in signaling pathways

İnme ve Terapötik Hipotermi

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