• Remote ischemic conditioning (RIC) is an experimental medical procedure that aims to reduce the severity of ischaemic injury to an organ such as the heart or the brain, most commonly in the situation of a heart attack or a stroke, or during procedures such as heart surgery when the heart may temporary suffer ischaemia during the operation, by triggering the body's natural protection against tissue injury. (wikipedia.org)
  • Excessive glutamate release and the overexcitation of glutamate receptors has been identified as a central mediator in the pathophysiology of the neuronal injury associated with ischemic stroke and head trauma ( Choi, 1987 ). (jneurosci.org)
  • Stroke is a disorder of blood vessels, which can affect neurons and cause ischemic brain injuries. (molcells.org)
  • Ischemic stroke is a vascular disorder affecting neuronal function. (molcells.org)
  • the EV-derived miRNAs are able to engage in regulation of protein expression and thereby interfere with cellular degradation in remote tissues suffering from chronic ischemia or inflammation (e.g. myocardial infarct, stroke, ulcerative colitis or muscle metabolism). (au.dk)
  • Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats. (ac.ir)
  • 9. Allahtavakoli M, Moloudi R, Arababadi MK, Shamsizadeh A, Javanmardi K. Delayed post ischemic treatment with Rosiglitazone attenuates infarct volume, neurological deficits and neutrophilia after embolic stroke in rat. (ac.ir)
  • 21. Zhao H. Ischemic postconditioning as a novel avenue to protect against brain injury after stroke. (ac.ir)
  • Della-Morte, D. Polyphenols and Ischemic Stroke. (encyclopedia.pub)
  • Polyphenols and Ischemic Stroke" Encyclopedia , https://encyclopedia.pub/entry/11184 (accessed December 07, 2023). (encyclopedia.pub)
  • Two main types of stroke exist: ischemic stroke (due to clot-mediated blood vessel occlusion), which accounts for about 85% of all stroke cases, and hemorrhagic stroke (caused by blood vessel rupture), which accounts for 15% of total cases. (encyclopedia.pub)
  • 12. Mitsios N, Gaffney J, Kumar P, Krupinski J, Kumar S, Slevin M. Pathophysiology of acute ischaemic stroke: an analysis of common signalling mechanisms and identification of new molecular targets. (southampton.ac.uk)
  • Pathobiology of ischaemic stroke: an integrated view. (southampton.ac.uk)
  • Ischemic stroke is a highly prevalent condition that frequently results in life-long disability and death. (explorationpub.com)
  • Considerable efforts have been made to establish treatments that prevent secondary ischemic damage and promote stroke recovery. (explorationpub.com)
  • The most common type of stroke is ischemic stroke, which results from the occlusion of a cerebral vessel by a clot. (explorationpub.com)
  • Despite the extensive attempts in developing ischemic stroke treatments, only intravenous thrombolysis and endovascular thrombectomy have hitherto been shown to be effective in clinical settings. (explorationpub.com)
  • Ischemic stroke activates components of innate and/or adaptive immunity and induces brain inflammatory responses, which besides removing damaged tissue exacerbate ischemic brain injury [ 3 , 4 ]. (explorationpub.com)
  • Specifically, polymorphonuclear neutrophils (PMNs) have been shown to play a critical role in the exacerbation of ischemic brain injury in the acute stroke phase and in the postischemic brain remodeling and angiogenesis in the post-acute phase [ 5 , 6 ]. (explorationpub.com)
  • It has been shown that NR2A/B is the only marker with high negative and positive predictive value in people with suspected ischaemic stroke. (annaly-nevrologii.com)
  • Temporary occlusion (120 min) of the right middle cerebral artery was induced 4 days after preconditioning and the infarct volume was measured. (elsevierpure.com)
  • Global cerebral ischemia was performed via 10 min of four-vessel occlusion. (springer.com)
  • transient sub-lethal ischemia and/or occlusion-reperfusion inherent of intermittent occlusion of blood flow at rest (RIC) or during exercise (BFRE), constitute the initial stimuli to promote release of molecular signals. (au.dk)
  • release signals consist of extracellular vesicle (EV)-derived miRNA released from cells at the origin of ischemia/occlusion that circulates to remote organs. (au.dk)
  • Transient ischemic attack (TIA) is a transient neurological deficit (speech disturbance, weakness…), caused by temporary occlusion of a brain vessel by a blood clot that leaves no lasting effect. (stanford.edu)
  • ENGLISH ABSTRACT: The Mechanism of -adrenergic preconditioning ( -PC) Ischaemic preconditioning (IPC), a potent endogenous protective intervention against myocardial ischaemia, is induced by exposure of the heart to repetitive short episodes of ischaemia and reperfusion. (sun.ac.za)
  • remote ischemic conditioning reduced infarct size in ST-elevation myocardial infarction (STEMI) patients when used in the ambulance or emergency department as an adjunct therapy to primary percutaneous coronary intervention (PCI), or when used with thrombolytic drugs. (wikipedia.org)
  • Remote ischemic preconditioning (RIPC) may confer the protection in critical organs. (silverchair.com)
  • Ren C, Yan Z, Wei D et al (2009) Limb remote ischemic postconditioning protects against focal ischemia in rats. (springer.com)
  • Intriguingly, a systemic protective response can be induced by repeated brief ischemia of a limb (remote ischemic conditioning, RIC). (au.dk)
  • Working model of remote ischemic conditioning (RIC) and blood flow restricted resistance exercise (BFRE) . (au.dk)
  • 2. Ren C, Yan Z, Wei D, Gao X, Chen X, Zhao H. Limb remote ischemic postconditioning protects against focal ischemia in rats. (ac.ir)
  • Protected phenotypes arise with both pre- and post-ischemic treatment with A3AR agonists, and transient A3AR agonism also triggers early and delayed preconditioned states. (edu.au)
  • The production of antioxidant enzymes that scavenge free radicals in ischemic tissue is then impaired, thereby exacerbating the damage caused by these free radicals in the post ischemic reperfusion tissue. (frontiersin.org)
  • We found remifentanil postconditioning markedly improved the spatial learning and memory as well as attenuated neuronal apoptosis in hippocampus caused by cerebral ischemia/reperfusion injury. (springer.com)
  • Neuroinflammation is one of the key pathological events involved in the progression of brain damage caused by cerebral ischemia. (southampton.ac.uk)
  • Ischaemic preconditioning describes the phenomenon where transient and brief ischaemia confers protection against a subsequent prolonged and injurious period of ischaemia. (medsci.org)
  • Here we investigated whether remifentanil postconditioning exerts neuroprotective effects against global cerebral ischemia/reperfusion injury in rats and its potential mechanisms. (springer.com)
  • The results suggest that remifentanil postconditioning exhibits neuroprotective effects against global cerebral ischemia/reperfusion injury in rats, and its mechanisms might involve inhibition of neuronal apoptosis through the PI3K pathway. (springer.com)
  • Wang JY, Shen J, Gao Q et al (2008) Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats. (springer.com)
  • Ding ZM, Wu B, Zhang WQ et al (2012) Neuroprotective Effects of Ischemic Preconditioning and Postconditioning on Global Brain Ischemia in Rats through the same effect on inhibition of apoptosis. (springer.com)
  • Chen TY, Goyagi T, Toung TJ et al (2004) Prolonged opportunity for ischemic neuroprotection with selective kappa-opioid receptor agonist in rats. (springer.com)
  • Zhang Y, Chen ZW, Girwin M et al (2005) Remifentanil mimics cardioprotective effect of ischemic preconditioning via protein kinase C activation in open chest of rats. (springer.com)
  • Jeong S, Kim SJ, Jeong C et al (2012) Neuroprotective effects of remifentanil against transient focal cerebral ischemia in rats. (springer.com)
  • We have shown that preconditioning by lipopolysaccharide (LPS) will result in 90% reduction in ischemic brain damage in P7 rats. (biomedcentral.com)
  • 4. Ren C, Gao X, Niu G, Yan Z, Chen X, Zhao H. Delayed postconditioning protects against focal ischemic brain injury in rats. (ac.ir)
  • Ischemic postconditioning may not influence early brain injury induced by focal cerebral ischemia/reperfusion in rats. (ac.ir)
  • 13. Zhang W, Miao Y, Zhou S, Jiang J, Luo Q, Qiu Y. Neuroprotective effects of ischemic postconditioning on global brain ischemia in rats through upregulation of hippocampal glutamine synthetase. (ac.ir)
  • In two models of partial renal IR with and without ischemia preconditioning (IPC) and using Mas receptor (MasR) blockade, A779 or its vehicle, the renal vascular responses to angiotensin II (Ang II) administration in two-kidney-one-clip (2K1C) hypertensive rats were determined. (hindawi.com)
  • The rats in the IR group underwent 45 min partial kidney ischemia, and the animals in the IPC + IR group underwent two 5 min cycles of partial kidney ischemia followed by 10 min reperfusion and partial kidney ischemia for 45 min. (hindawi.com)
  • We examined the effect of L-NAME, an inhibitor of NO synthase, on CSD-induced tolerance against transient focal cerebral ischemia. (elsevierpure.com)
  • The fate of the brain tissue after focal cerebral ischemia is determined by the degree and duration of ischemia, and even without preconditioning, resident brain cells naturally respond to brain ischemia by mobilizing a host of defences and counter responses to mitigate cell injury and death [ 5 ]. (biomedcentral.com)
  • 6. Xing B, Chen H, Zhang M, Zhao D, Jiang R, Liu X, Zhang S. Ischemic postconditioning inhibits apoptosis after focal cerebral ischemia/reperfusion injury in the rat. (ac.ir)
  • In animal models, focal mechanisms without evidence of macro-reentry play a major role in the origin of ventricular arrhythmia associated with ischemic cardiomyopathy. (medscape.com)
  • The A3 adenosine receptor (A3AR) is attributed with multiple beneficial actions in ischemic-reperfused myocardium, including modulation of oncotic and apoptotic cell death and enhancement of contractile function. (edu.au)
  • This coupled comorbidity of pathological ischemia and therapeutic reinjury of infarcted myocardium, namely, myocardial ischemia-reperfusion injury (MIRI), is particularly refractory to treatment [ 4 , 5 ]. (hindawi.com)
  • 9. Sasayama S, Nonogi H , Fujita M, Sakurai T, Wakabayashi A, Kawai C, Eiho S, Kuwahara M: Changes in diastolic properties of the regional myocardium during pacing-induced ischemia in human subjects. (fiercecert.com)
  • Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium. (medscape.com)
  • When the lethal ischemic insult is applied onto this latent protective phenotype, a separate set of responses are triggered that constitute ischemia-tolerant phenotype, which strikingly differs from the unprimed or unpreconditioned brain's phenotype (Figure 1 ). (biomedcentral.com)
  • Ischemic preconditioning (IPC) is normally an ailment of sublethal transient global ischemia and exhibits neuroprotective effects against following lethal ischemic insult. (biodiversityhotspot.org)
  • Alkan T (2009) Neuroproctective effects of ischemic tolerance (preconditioning) and postconditioning. (springer.com)
  • We characterized a glucose dependent hyperpolarization of the mitochondrial membrane potential (Δψ m ) in the majority of neurons after transient glutamate excitation. (jneurosci.org)
  • Delayed postconditionig initiates additive mechanism necessary for survival of selectively vulnerable neurons after transient ischemia in rat brain. (ac.ir)
  • Cortical spreading depression (CSD) has been documented to confer ischemic tolerance on brain. (elsevierpure.com)
  • Ischemic tolerance defines transient resistance to lethal ischemia gained by a prior sublethal noxious stimulus (i.e., preconditioning). (biomedcentral.com)
  • Since the first landmark experimental demonstration of ischemic tolerance in the gerbil brain in early 1990's, basic scientific knowledge on the mechanisms of cerebral ischemic tolerance increased substantially. (biomedcentral.com)
  • Ischemic tolerance occurs in two temporally distinct windows. (biomedcentral.com)
  • In humans, transient ischemic attacks may be the clinical correlate of preconditioning leading to ischemic tolerance. (biomedcentral.com)
  • This phenomenon named as preconditioning (PC) and tolerance has been shown to exist in many organs, most extensively in the heart. (biomedcentral.com)
  • 2018). Resveratrol Preconditioning Induces Genomic and Metabolic Adaptations within the Long-Term Window of Cerebral Ischemic Tolerance Leading to Bioenergetic Efficiency . (kolabtree.com)
  • 2017). Neuronal SIRT1 (Silent Information Regulator 2 Homologue 1) Regulates Glycolysis and Mediates Resveratrol-Induced Ischemic Tolerance . (kolabtree.com)
  • Ischemic tolerance or preconditioning is a phenomenon by which a sub-injurious stimulus is applied to a tissue such as the brain. (biomedcentral.com)
  • After a certain delay, the brain develops tolerance to ischemic injury caused by the injurious stimulus. (biomedcentral.com)
  • The neuroprotective effects of remifentanil preconditioning against cerebral ischemia/reperfusion injury have been recently reported. (springer.com)
  • Finally, we will provide a critical evaluation of the therapeutic potential of COX inhibitors in cerebral ischemia and discuss new targets downstream of COX with potential neuroprotective ability. (southampton.ac.uk)
  • We hypothesized that TLRs other than TLR-4 may mediate preconditioning against cerebral ischemic injury in the developing brain. (biomedcentral.com)
  • Three cycles of 5-min ischemia/5-min reperfusion induced by a blood pressure cuff served as RIPC stimulus. (silverchair.com)
  • In the scenario of IT, PC stimulus primes the brain for subsequent injurious ischemic injury. (biomedcentral.com)
  • Danger signal evoked in the brain by the stressing preconditioning stimulus induces complex endogenous protective mechanisms resulting to a latent protective phenotype. (biomedcentral.com)
  • At 48 h after the injections, hypoxic-ischemic (HI) injury was induced by unilateral carotid artery ligation followed by hypoxia for 65 min. (biomedcentral.com)
  • The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)
  • Nonetheless, A3ARs may be more promising as therapeutic "anti-ischemic" targets compared with other adenosine receptor subtypes, since A3AR agonists elicit fewer and less significant side-effects. (edu.au)
  • Despite significant advances in therapeutic techniques ischemic cardiovascular disease remains the leading cause of mortality and heart failure in most countries [1]. (immune-source.com)
  • 14. Sun X, Fang B, Zhao X, Zhang G, Ma H. Preconditioning of mesenchymal stem cells by sevoflurane to improve their therapeutic potential. (sciendo.com)
  • These therapeutic effects can be further enhanced by hypoxic preconditioning. (researchsquare.com)
  • and even more difficult is to assess the therapeutic effects of such a transient state.1,2 These mesomeric states create a conundrum within the scientific community. (diegovitello.it)
  • Endogenous release of adenosine during ischemic/remote preconditioning or exogenous adenosine during pharmacological preconditioning activates adenosine receptors to activate plethora of mechanisms, which either independently or in association with one another may confer cardioprotection during ischemia-reperfusion injury. (kyobobook.co.kr)
  • We will discuss issues related to the biochemistry and selective pharmacological inhibition of COX enzymes, and further refer to their expression in the brain under normal conditions and following excitotoxicity and ischemic cerebral injury. (southampton.ac.uk)
  • 10. Frässdorf J, De Hert S, Schlack W. Anaesthesia and myocardial ischaemia/reperfusion injury. (sciendo.com)
  • Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings. (frontiersin.org)
  • 18. Wang CX, Yang T, Shuaib A. An improved version of embolic model of brain ischemic injury in the rat. (ac.ir)
  • We will review present knowledge of the relative contribution of each COX isoform to the brain ischemic pathology, based on data from investigations utilizing selective COX-1/COX-2 inhibitors and genetic knockout mouse models. (southampton.ac.uk)
  • Charron C, Messier C, Plamondon H (2008) Neuroprotection and functional recovery conferred by administration of kappa- and delta 1-opioid agonists in a rat model of global ischemia. (springer.com)
  • 6) was put through 30 min of global ischemia accompanied by 180 min of reperfusion. (immune-source.com)
  • Adenosine also serves as an important trigger in ischemic and remote preconditioning and its release may impart cardioprotection. (kyobobook.co.kr)
  • Exogenous administration of adenosine in the form of adenosine preconditioning may also protect heart from ischemia-reperfusion injury. (kyobobook.co.kr)
  • The present review discusses the role and mechanisms involved in adenosine preconditioning-induced cardioprotection. (kyobobook.co.kr)
  • Available evidence indicates that this receptor sub-type is minimally activated by endogenous adenosine during ischemia (A3AR antagonists exerting no effects on ischemic outcome), and is thus amenable to activation with exogenous agonists. (edu.au)
  • the respective roles of the A1-, A2-, A3-adenosine receptors as well as the involvement of the PI3-K/PKB/Akt and ERKp44/p42 signal transduction pathways, in the cardioprotective phenomemon of -adrenergic preconditioning and (iv) the contribution of the mitochondrial KATP channels (mKATP), reactive oxygen species and NO to the mechanism of -AR-induced cardioprotection. (sun.ac.za)
  • Neurons and microvessels respond equally rapidly to the acute ischemic insult. (molcells.org)
  • During the acute phase of cerebral ischemia, vascular injury mainly refers to cerebral microvascular system, which results in increased Blood Brain Barrier permeability. (molcells.org)
  • Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. (frontiersin.org)
  • Partial kidney ischemia-reperfusion (IR) injury is the principal cause of acute kidney injury. (hindawi.com)
  • Key studies are reviewed that have demonstrated the possibility of using glutamate receptors and their antibodies as potential biomarkers of acute and chronic cerebral ischemia. (annaly-nevrologii.com)
  • Cyclooxygenase inhibition in ischemic brain injury. (southampton.ac.uk)
  • Metabolism of arachidonic acid through cyclooxygenase (COX) enzymes is known to be actively involved in the neuroinflammatory events leading to neuronal death after ischemia. (southampton.ac.uk)
  • Ischaemic reperfusion injury (IRI) after tourniquet release during total knee arthroplasty (TKR) is related to postoperative cerebral complications. (medsci.org)
  • Tourniquet release during the late period of TKR can induce ischaemic-reperfusion injury, eliciting the activation of neutrophils, circulating pro-inflammatory cytokines, and reactive oxygen species [ 2 , 3 ]. (medsci.org)
  • Considering that tourniquet application during TKR is related to ischaemic injury, the organ protective effect of ischaemic preconditioning can have a beneficial role after tourniquet release during TKR. (medsci.org)
  • Zhang Y, Irwin MG, Wong TM (2004) Remifentanil preconditioning protects against ischemic injury in the intact rat heart. (springer.com)
  • Yuan Y, Guo Q, Ye Z et al (2011) Ischemic postconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt pathway. (springer.com)
  • Poly I:C-induced preconditioning against ischemic injury may be mediated by modulation of TLR-3 signaling pathways. (biomedcentral.com)
  • This is the first study to show that TLR-3 is expressed in the immature brain and mediates preconditioning against ischemic injury. (biomedcentral.com)
  • The expression of TLRs and their role in inflammation and ischemic injury in the adult brain is well documented. (biomedcentral.com)
  • Taken together, these results indicate the TLRs play an important role in ischemia-induced injury in the adult brain. (biomedcentral.com)
  • However, the role of TLRs in ischemic injury of the developing brain is yet to be determined. (biomedcentral.com)
  • Ischemic preconditioning, therefore, protects against subsequent ischemic injury. (biomedcentral.com)
  • While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. (hindawi.com)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • Many studies have focused on the roles of CSMCs in ischemic brain injury to investigate their functions and underlying mechanisms. (molcells.org)
  • In heart transplantation, donor hearts inevitably suffer from ischemia/reperfusion (I/R) injury, which leads to primary graft dysfunction and affects patients' survival rate. (researchsquare.com)
  • Bone marrow mesenchymal stem cells (BMSCs) have been reported to attenuate myocardial I/R injury via their paracrine effects, which can be enhanced by hypoxic preconditioning. (researchsquare.com)
  • Previous studies have shown that ischemia/reperfusion (I/R) injury acts as a significant role in PGD(4), contributing to adverse short- and long-term clinical outcomes in the recipients. (researchsquare.com)
  • 7. Yuan Y, Guo Q, Ye Z, Pingping X, Wang N, Song Z. Ischemic postconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt pathway. (ac.ir)
  • Kidney partial ischemia-reperfusion (IR) injury is defined as a reduction of the renal blood flow (RBF) followed by the recovery of RBF and reoxygenation [ 1 ]. (hindawi.com)
  • IPC is described as short, transient, and nonlethal ischemia periods and subsequent reperfusion which is performed before IR injury and can protect the kidney against long-term ischemia [ 6 - 8 ]. (hindawi.com)
  • As a result, transient hypotension and acidosis can occur [ 4 , 5 ], and serious cerebral complications can be induced [ 3 , 6 , 7 ]. (medsci.org)
  • Sinus tachycardia is associated with enhanced sympathetic activity and can result in transient hypertension or hypotension. (medscape.com)
  • The mechanisms of neurotoxicity associated with increased COX activity after ischemia will also be examined. (southampton.ac.uk)
  • Remote ischaemic preconditioning (RIPC) is known to minimise IRI in previous studies. (medsci.org)
  • Meanwhile, the organ protective effect of ischaemic preconditioning could be induced when the episodic ischaemia is at distant tissues or organs, the concept being termed remote ischaemic preconditioning (RIPC) [ 9 ]. (medsci.org)
  • The application of RIPC into clinical fields is more useful than ischaemic preconditioning because it is easy to apply briefly preceding ischaemia to distant organs such as the limbs. (medsci.org)
  • A similar systemic protective effect seems achievable by traditional exercise regimens while ischemic resistance exercise training conducted as low-intensity blood flow restricted resistance exercise (BFRE) holds the potential to promote tissue rebuilding by repeated application. (au.dk)
  • Volatile anesthetic-induced cardiac preconditioning. (sciendo.com)
  • Various noxious stimuli can precondition the brain, presumably through a common mechanism, genomic reprogramming. (biomedcentral.com)
  • The delay to protection may be minutes to few hours (rapid or early preconditioning) or days (delayed preconditioning) requiring protein synthesis [ 10 - 12 ]. (biomedcentral.com)
  • The clinician must be aware of these arrhythmias, in addition to reperfusion strategies, and must treat those that require intervention to avoid exacerbation of ischemia and subsequent hemodynamic compromise. (medscape.com)
  • The transient receptor potential cation channel subfamily M member 4 (TRPM4) is really a potential target because of this strategy. (immune-source.com)
  • However, it is not easy to apply ischaemic preconditioning in a clinical setting because brief organ ischaemia should be preceded after real ischaemic time [ 8 ]. (medsci.org)
  • The microvascular and parenchymal organ damage induced upon ischemia tissue reperfusion is mainly attributed to the reactive oxygen-free radicals, and it has been demonstrated in many organs. (frontiersin.org)