Ischaemic preconditioning of the brain, mechanisms and applications

Steiger, Hans‐Jakob; Hänggi, Daniel

doi:10.1007/s00701-006-1057-1

Cited by 97 publications

(81 citation statements)

References 62 publications

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“…These mediators can be induced only by low doses of NMDA via the action potential-dependent route [13,14] . CREB is a transcription factor that is activated in response to intracellular calcium elevation regulated by NMDA receptor activation [15] .…”

Section: Excitatory/inhibitory Neurotransmitters and Neuroprotectionmentioning

confidence: 99%

“…Since it can block apoptosis, thereby promoting cell survival, Akt has been implicated as a major factor in tumorigenesis in many types of cancer. Akt can be activated by phosphatidylinositol 3-kinase (PI-3K), so the PI-3K antagonists wortmannin and LY294002 may induce apoptotic signals by inhibiting Akt activation [14,37] . Recent evidence demonstrates the involvement of the activation of Akt in ischemic tolerance.…”

Section: Inflammatory Cytokinesmentioning

confidence: 99%

“…Chen et al [52] reported that thermal preconditioning with 44 o C body temperature protected cerebellar granule neurons of rats by modulating HSP70 expression. HSP70 mRNA was detected after thermal preconditioning at 30, 60, and 90 min and increased gradually with time, whereas HSP70 antisense oligodeoxynucleotides inhibited the protective effects of thermal preconditioning against apoptosis [14,52] . All these results implicate that HSP70 is an important player in the preconditioning process.…”

Section: Heat Shock Proteins (Hsps)mentioning

confidence: 99%

“…They showed that NO production and activity were critical to the induction of ischemic tolerance and that endothelial nitric oxide synthase (eNOS), not neuronal nitric oxide synthase (nNOS) or inducible nitric oxide synthase (iNOS), was the isoform responsible for producing ischemic tolerance. In the study by Sunghee Cho and his colleagues, both inhibiting nitric oxide synthase (NOS) and scavenging NO during preconditioning significantly attenuated the induced ischemic tolerance, however, neither eNOS nor nNOS knockout mice demonstrated altered ischemic preconditioning [14,69,70] . Meanwhile, preconditioning by volatile anesthetics also appears to involve the NO pathway.…”

Section: Nitric Oxide/reactive Oxygen Species and Neuroprotectionmentioning

confidence: 99%

“…Meanwhile, preconditioning by volatile anesthetics also appears to involve the NO pathway. Kapinya and coworkers showed that tolerance against ischemic neuronal injury in rats can be induced by volatile anesthetics and that this effect is dependent on iNOS [14,71] .…”

Section: Nitric Oxide/reactive Oxygen Species and Neuroprotectionmentioning

confidence: 99%

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The neuroprotective mechanism of brain ischemic preconditioning

2009

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Brain ischemia is one of the most common causes of death and the leading cause of adult disability in the world. Brain ischemic preconditioning (BIP) refers to a transient, sublethal ischemia which results in tolerance to later, otherwise lethal, cerebral ischemia. Many attempts have been made to understand the molecular and cellular mechanisms underlying the neuroprotection offered by ischemic preconditioning. Many studies have shown that neuroprotective mechanisms may involve a series of molecular regulatory pathways including activation of the N-methyl-D-aspartate (NMDA) and adenosine receptors; activation of intracellular signaling pathways such as mitogen activated protein kinases (MAPK) and other protein kinases; upregulation of Bcl-2 and heat shock proteins (HSPs); and activation of the ubiquitin-proteasome pathway and the autophagic-lysosomal pathway. A better understanding of the processes that lead to cell death after stroke as well as of the endogenous neuroprotective mechanisms by which BIP protects against brain ischemic insults could help to develop new therapeutic strategies for this devastating neurological disease. The purpose of the present review is to summarize the neuroprotective mechanisms of BIP and to discuss the possibility of mimicking ischemic preconditioning as a new strategy for preventive treatment of ischemia.

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Section: Excitatory/inhibitory Neurotransmitters and Neuroprotectionmentioning

confidence: 99%

Section: Inflammatory Cytokinesmentioning

confidence: 99%

Section: Heat Shock Proteins (Hsps)mentioning

confidence: 99%

Section: Nitric Oxide/reactive Oxygen Species and Neuroprotectionmentioning

confidence: 99%

Section: Nitric Oxide/reactive Oxygen Species and Neuroprotectionmentioning

confidence: 99%

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The neuroprotective mechanism of brain ischemic preconditioning

2009

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Predicting hemorrhagic transformation and its timing from maximum cerebral lesion diameter in nonlacunar ischemic strokes

et al. 2019

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ObjectivesWe performed this retrospective cohort study to establish which factors are mostly indicative of the appearance of hemorrhagic transformation (HT) and of its time course in a sample of nonlacunar ischemic strokes.Materials and MethodsIn 402 patients with nonlacunar ischemic stroke (75.0 ± 12.7 years, 192 male), clinical, laboratory, and neuroimaging variables obtained during the first 3 days of hospitalization were compared between patients with and without HT at computer tomography scan.ResultsHT was documented in 129 patients (32.1%), including 36 with parenchymal hematoma (PH), after a median time of 6 days (range 1–27). Many variables were univariately associated with HT, but only 5 of them were confirmed in Cox regression (Hazard Ratio, 95% Confidence Interval): maximum cerebral lesion diameter (CLD) in cm (1.12, 1.06–1.18; p = .0001), hemoglobin in g/dl (1.16, 1.06–1.27; p = .002), blood glucose in mmol/L (1.10, 1.03–1.18; p = .007), prior anticoagulant therapy (1.82, 1.10–3.03; p = .02), and edema with mass effect (1.72, 1.08–2.75; p = .02). Thus, the most significant predictor was CLD. The overall risk of HT was minimum for CLD < 2 cm (1.5%), intermediate for CLD ≥ 2 and < 5 cm (22%), and maximum for CLD ≥ 5 cm (58%). The residual probability of having HT decreased progressively over time, and a simple formula is proposed to predict, from CLD in cm, when the probability of HT falls below 10%.ConclusionsThe main determinant of HT was CLD, a simple quantitative parameter that could prove useful, in particular, in deciding the timing of anticoagulation in cardioembolic stroke patients.

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GAPDH in Anesthesia

Seidler

2012

GAPDH: Biological Properties and Diversity

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Thus far, two independent laboratories have shown that inhaled anesthetics directly affect GAPDH structure and function. Additionally, it has been demonstrated that GAPDH normally regulates the function of GABA (type A) receptor. In light of these literature observations and some less direct findings, there is a discussion on the putative role of GAPDH in anesthesia. The binding site of inhaled anesthetics is described from literature reports on model proteins, such as human serum albumin and apoferritin. In addition to the expected hydrophobic residues that occupy the binding cavity, there are hydrophilic residues at or in very close proximity to the site of anesthetic binding. A putative binding site in the bacterial analog of the human GABA (type A) receptor is also described. Additionally, GAPDH may also play a role in anesthetic preconditioning, a phenomenon that confers protection of cells and tissues to future challenges by noxious stimuli. The central thesis regarding this paradigm is that inhaled anesthetics evoke an intra-molecular protein dehydration that is recognized by the cell, eliciting a very specific burst of chaperone gene expression. The chaperones that are implicated are associated with conferring protection against dehydration-induced protein aggregation.

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Ischaemic preconditioning of the brain, mechanisms and applications

Cited by 97 publications

References 62 publications

The neuroprotective mechanism of brain ischemic preconditioning

The neuroprotective mechanism of brain ischemic preconditioning

Predicting hemorrhagic transformation and its timing from maximum cerebral lesion diameter in nonlacunar ischemic strokes

GAPDH in Anesthesia

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