• Oral dosing of rats with SCN-, before acute ischemia-reperfusion injury (30 min occlusion, 24 h or 4 week recovery), significantly reduced the infarct size as a percentage of the total reperfused area (54% versus 74%), and increased the salvageable area (46% versus 26%) as determined by MRI imaging. (ku.dk)
  • We therefore investigated the impact of global brain hypoxia-ischemia on the thalamic circuit function in the somatosensory system of young rats. (cdc.gov)
  • Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. (frontiersin.org)
  • While developmental senescence and acute senescence may positively contribute to the fine-tuning of embryogenesis and injury repair, chronic senescence, when unresolved promptly, plays a crucial role in kidney fibrogenesis and CKD progression. (frontiersin.org)
  • These data indicate that elevated levels of the MPO substrate SCN-, which can be readily modulated by dietary means, can protect against acute ischemia-reperfusion injury. (ku.dk)
  • Here, we review the information linking the adaptor protein p66Shc with cardiac injury induced by ischaemia and reperfusion (I/R), including the contribution of risk factors, such as metabolic syndrome and ageing. (nih.gov)
  • Global brain hypoxia-ischemia during cardiac arrest has a long-term impact on processing and transfer of sensory information by thalamic circuitry. (cdc.gov)
  • If treated with cardiopulmonary resuscitation, however, cardiac arrest is survivable, but survivors often show evidence of injury in selectively vulnerable regions of the brain. (cdc.gov)
  • Ischaemic reperfusion injury (IRI) after tourniquet release during total knee arthroplasty (TKR) is related to postoperative cerebral complications. (medsci.org)
  • Previous studies of global brain hypoxia ischemia have primarily focused on injury to the cerebral cortex and to the hippocampus. (cdc.gov)
  • 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)
  • 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)
  • 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)
  • 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)
  • Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings. (frontiersin.org)
  • Ischaemic preconditioning describes the phenomenon where transient and brief ischaemia confers protection against a subsequent prolonged and injurious period of ischaemia. (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)
  • Taking N-acetyl cysteine by mouth seems to reduce homocysteine levels, a possible risk factor for heart disease. (medlineplus.gov)
  • Taking N-acetyl cysteine by mouth seems to reduce levels of a blood fat called lipoprotein(a) in people with high levels of this blood fat. (medlineplus.gov)
  • Global hypoxia-ischemia interrupts oxygen delivery and blood flow to the entire brain. (cdc.gov)
  • Is Aryl Hydrocarbon Receptor Antagonism After Ischemia Effective in Alleviating Hepatic Ischemia-Reperfusion Injury in Rats? (researchsquare.com)
  • Lung tissue necrosis after prolonged ischaemia is known to worsen lung function, which was believed to be due largely to adjacent tissue inflammation. (ersjournals.com)
  • Tissue necrosis after lung ischaemia-reperfusion injury has been recognised to be associated with significantly worsened lung function, related to the high degree of inflammation. (ersjournals.com)
  • 10 6 Since pain is a manifestation of complex sickle pathobiology including inflammation, vascular dysfunction and ischemia/reperfusion injury, we investigated cannabinoid receptor-specific modulation of vascular function, inflammation and hyperalgesia. (haematologica.org)
  • 19 Since vascular dysfunction, ischemia/reperfusion injury and inflammation are hallmark features of SCA, we hypothesized that targeting specific cannaboid receptors may have beneficial effects on sickle pathobiology and pain. (haematologica.org)
  • In conclusion, hypercholesterolemia could aggravate myocardial ischemia/reperfusion injury, attenuate cardioprotection of ischemic preconditioning and eliminate cardioprotection from α7nAChR agonist postconditioning by enhancing inflammation and inhibiting PI3K/Akt/eNOS pathway. (spandidos-publications.com)
  • I am interested in the role played by complememt in various types of kidney injury including, glomerular disease, interstitial inflammation and ischaemia reperfusion injury. (ncl.ac.uk)
  • While the goal of recanalisation therapy is very apparent and has good indicators for translation, cerebroprotection must ideally fulfil a multitude of purposes, including the improvement of cerebral microcirculation, the reduction of infarct progression, the tight regulation of metabolic processes, and the prevention of reperfusion injury, inflammation and haemorrhagic transformation. (bmj.com)
  • Ischemia/reperfusion injury in skeletal muscle leads to sterile inflammation and affects structure and function permanently. (bvsalud.org)
  • These involve the activation of Jak/STAT3 and PI3K/Akt, which subsequently decreases mitochondrial permeability transition pore (mPTP) opening and increases mitochondrial K ATP (Mito K ATP ) channel opening, which attenuates myocardial ischaemia reperfusion injury. (researchgate.net)
  • Myocardial ischaemia reperfusion injury is the leading cause of death in patients with cardiovascular disease. (researchgate.net)
  • Interventions such as ischaemic pre and postconditioning protect against myocardial ischaemia reperfusion injury. (researchgate.net)
  • as a feasible method for reduction of myocardial ischaemia-reperfusion (IR) injury. (researchgate.net)
  • Rossello X, Lobo-Gonzalez M and Ibanez B: Editor's choice-pathophysiology and therapy of myocardial ischaemia/reperfusion syndrome. (spandidos-publications.com)
  • Furthermore, the pharmacological inhibition of AhR activation after ischemia has been shown to attenuate cerebral ischemia-reperfusion (IR) injury. (researchsquare.com)
  • 9 Recent studies have suggested that cerebral ischemia induces AhR activation and exacerbates neuronal damage. (researchsquare.com)
  • This dissertation research focused on focal cerebral ischemia, using the middle cerebral artery occlusion model in rats and mice. (ncl.edu.tw)
  • After prolonged periods (up to 18 h) of cold ischaemic lung preservation without reperfusion, a high percentage of cell necrosis (but not apoptosis) can be observed 12 , 13 . (ersjournals.com)
  • Ischaemic postconditioning confers cardioprotection through the survivor activating factor enhancement (SAFE) and reperfusion injury salvage kinase (RISK) pathways. (researchgate.net)
  • Hausenloy DJ and Yellon DM: Ischaemic conditioning and reperfusion injury. (spandidos-publications.com)
  • We then outline the diverse, multicellular effects of ischaemic stroke and the complex temporal sequences of the pathophysiological cascade during and following ischaemia, reperfusion, and recovery. (bmj.com)
  • This may be explained by several factors that encompass practical considerations such as study design, implementation, and evaluation, focusing on a singular putative target in the ischaemic cascade or failing to consider potentially influencing factors such as the patient's reperfusion status. (bmj.com)
  • The central role of lung ischaemia-reperfusion injury in pulmonary dysfunction after cardiac surgery, particularly thoracic organ transplantation, has been well recognised. (ersjournals.com)
  • Recent studies suggest that lung apoptosis following ischaemia-reperfusion could be equally important in the development of post-operative lung dysfunction. (ersjournals.com)
  • The current literature on the mechanism and pathways involved in pulmonary dysfunction and, in particular, its relationship with apoptosis after lung ischaemia-reperfusion is briefly reviewed here. (ersjournals.com)
  • Ischaemia-reperfusion-induced pulmonary dysfunction is a significant clinical problem in cardiac surgery and, particularly, lung transplantation 1 . (ersjournals.com)
  • Post-operative pulmonary dysfunction following the use of cardiopulmonary bypass is a frequently observed phenomenon that is associated with lung ischaemia-reperfusion injury 2 , 3 . (ersjournals.com)
  • Pulmonary ischaemia-reperfusion can cause cellular breakdown and death of lung epithelial tissue, which may contribute to the magnitude and duration of pulmonary dysfunction seen after cardiopulmonary bypass and lung transplantation 2 , 4 . (ersjournals.com)
  • Hepatic ischemia-reperfusion (IR) injury commonly occurs during liver transplantation or resection and is considered a leading cause of liver damage and dysfunction. (researchsquare.com)
  • Wu Y, Liu H and Wang X: Cardioprotection of pharmacological postconditioning on myocardial ischemia/reperfusion injury. (spandidos-publications.com)
  • Andreadou I, Iliodromitis EK, Lazou A, Görbe A, Giricz Z, Schulz R and Ferdinandy P: Effect of hypercholesterolaemia on myocardial function, ischaemia-reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning. (spandidos-publications.com)
  • In isolated rat hearts, IPo stimulation reduced post-is- chaemic infarct size with associated elevations in Akt, eNOS, and p70S6K, while these beneficial effects of IPo were abolished by PI3K inhibition (either by LY294002 or wortmannin), indicating the involvement of PI3K-Akt in IPo. (researchgate.net)
  • Since the mid-1980s, the role of neutrophils, free radicals and other inflammatory mediators in ischaemia-reperfusion injury has been extensively investigated 4 . (ersjournals.com)
  • Since the late 1990s, scientists have recognised that the different processes following ischaemia-reperfusion, although closely related, cause lung injury by activation of different inflammatory pathways 2 , 4 , 6 . (ersjournals.com)
  • 5 4 Cannabinoids have anti-inflammatory effects and provide protection from ischemia/reperfusion injury. (haematologica.org)
  • Xiong J, Yuan YJ, Xue FS, Wang Q, Cheng Y, Li RP, Liao X and Liu JH: Postconditioning with α7nAChR agonist attenuates systemic inflammatory response to myocardial ischemia-reperfusion injury in rats. (spandidos-publications.com)
  • Negative pressure wound therapy reduces the ischaemia/reperfusion-associated inflammatory response in free muscle flaps. (leading-medicine-guide.com)
  • A pharmacological agent that could reduce the risk of IRI and prolong the "safe" warm ischemia time would cause a global transformational change in the utilization of partial nephrectomy, with broader implications for renal transplantation, cardiac surgery, and the myriad other surgeries that involve IRI. (hindawi.com)
  • 10 Moreover, the pharmacological manipulation of AhR activation after ischemia has been shown to modulate neuronal damage due to cerebral IR in vivo . (researchsquare.com)
  • However, understanding of the complex pathophysiology of ischaemia-reperfusion-induced lung injury remains incomplete. (ersjournals.com)
  • Targeting HIF-1α to Prevent Renal Ischemia-Reperfusion Injury: Does It Work? (hindawi.com)
  • This is a time-critical step due to the critical ischemia period of renal tissue. (hindawi.com)
  • Prolonged renal ischemia may lead to irreversible nephron damage in the remaining tissue and, ultimately, chronic kidney disease. (hindawi.com)
  • The aim of this review is to highlight the techniques and drugs that target HIF-1 α and ameliorate IRI associated with renal ischemia. (hindawi.com)
  • The two key factors that contribute to postoperative loss of renal function are ischemia time and degree of parenchymal loss [ 2 ]. (hindawi.com)
  • Beyond this period, critical ischemia ensues, where renal cells are irreversibly injured, eventually resulting in nephron loss and chronic kidney disease in 5-17% patients [ 4 ]. (hindawi.com)
  • Progression to renal damage by ischemia-reperfusion injury (IRI) is the result of the dysregulation of various tissue damage repair mechanisms. (researchgate.net)
  • 1 - 5 The mechanisms of hepatic IR injury have been extensively investigated, but nevertheless remain largely unclear. (researchsquare.com)
  • Recently, the mechanisms involved in pulmonary apoptosis following lung ischaemia-reperfusion have begun to be understood 5 . (ersjournals.com)
  • This is potentiated by the incompletely understood ischemia-reperfusion injury (IRI). (hindawi.com)
  • Ischemia-reperfusion injury (IRI) is a syndrome affecting the myocardium upon blood flow restoration following a sufficiently long interruption, such as encountered in a coronary thrombosis or heart surgery [1,2]. (justia.com)
  • In the present study, we investigated the protective effects of AhR antagonism after ischemia in a rat hepatic IR injury model. (researchsquare.com)
  • The present invention is based on the surprising finding that the peptides of the invention have protective cardiovascular effects without simultaneous administration of other compounds, specifically they have protective effects on the heart against ischemia-reperfusion injury. (justia.com)
  • In experimental studies of rodent single-lung transplantation, a short duration of ischaemia (20 min) and reperfusion was associated with neither increased cellular necrosis nor apoptosis of the transplanted lung compared with the pre-retrieval lungs 12 . (ersjournals.com)
  • Nevertheless, these mediators appear to contribute only in part to lung ischaemia-reperfusion injury. (ersjournals.com)
  • Aryl hydrocarbon receptors (AhRs) have been reported to be important mediators of ischemic injury in the brain. (researchsquare.com)
  • Excessive activation can lead to to tissue injury. (ncl.ac.uk)
  • Iatrogenic revascularization and restoration of perfusion results paradoxically in aggravated tissue injury. (bvsalud.org)
  • Monitoring molecular changes induced by ischemia/reperfusion in human free muscle flap tissue samples. (leading-medicine-guide.com)
  • However, while the majority of cancers are suitable for partial nephrectomy, concern about the warm ischemia time has meant that only around 25% of small kidney cancers are treated with nephron-sparing surgery [ 3 ]. (hindawi.com)
  • However, to the best of our knowledge, the effects of AhR antagonism on hepatic IR injury have not yet been reported. (researchsquare.com)
  • 10 , 11 This is because L-kynurenine (L-Kyn), an endogenous ligand of AhR, is accumulated in the brain during ischemia and triggers the activation of AhR. (researchsquare.com)
  • Therefore, the inhibition of AhR activation after ischemia is considered to be effective in suppressing hepatic IR injury. (researchsquare.com)
  • The invention pertains to a polypeptide for the protection against heart ischemia-reperfusion injury. (justia.com)
  • One object of the present invention is to provide a therapy of heart ischemia-reperfusion injury by applying GLP-1 analogues which can be administered as single component and avoiding administration of the drug with a second compound. (justia.com)
  • Postconditioning using N-Ac-GLP-1(7-34)amide N-terminally blocked and C-terminally truncated results in a limitation of ischemia-reperfusion injury in an isolated rat heart. (justia.com)
  • Although a large number of drugs and agents (including Ca 2+ -channel blockers, mannitol, acadesine, adenosine, Na + /H + -exchange inhibitors, and N-acetylcysteine (an antioxidant)) have been shown to protect against ischemia-reperfusion injury (IRI) in the kidney in vitro and in vivo (in either rat or mouse), all have failed in either large animal or human trials [ 5 - 8 ]. (hindawi.com)
  • Previous studies have shown that intracerebral administration of glial cell line-derived neurotrophic factor (GDNF) reduces ischemia-mediated cerebral infarction. (ncl.edu.tw)
  • Hepatic IR injury was observed using serum, magnetic resonance imaging-based liver function indices, and liver samples. (researchsquare.com)
  • Because L-Kyn is produced in a significant amount in the liver through the degradation of L-tryptophan by tryptophan-2,3-dioxygenase (TDO), 13 it is more likely to accumulate in the liver than in the brain due to ischemia. (researchsquare.com)
  • Unlike any other organ in the human body, the lung possesses two blood supply networks with extensive anastomotic connections and a total of three potential sources of lung tissue oxygenation, thus making lung ischaemia-reperfusion injury more intriguing to study 2 . (ersjournals.com)
  • This chapter will provide a detailed experimental setup and a step-by-step protocol for the dynamic imaging of leukocyte-endothelial-interaction in an ischemia/reperfusion injury model. (bvsalud.org)
  • This figure outlines the time course for normoxic (A) and ischemia-reperfusion (B) experiments. (justia.com)
  • Upregulating HIF-1 α via ischemic preconditioning (IPC) or drugs that simulate hypoxia (hypoxia-mimetics) has been investigated as a method to reduce IRI. (hindawi.com)
  • 7 8 Indeed, many drugs that were unable to show a treatment effect in the pre-endovascular thrombectomy (EVT) era, in which most patients were not reperfused, may be more potent when administered as a bridge to save tissue before EVT reperfusion or when administered to rescue tissue after EVT, directly into the reperfused brain. (bmj.com)
  • Serum lactate dehydrogenase (LDH), creatine kinase isoenzyme MB (CK-MB), cardiac troponin I (cTnI), tumor necrosis factor α (TNF‑α) and interleukin‑6 (IL‑6) levels after ischemia/reperfusion were assayed. (spandidos-publications.com)
  • Animals were sacrificed at 0, 6, 12, and 24 h after reperfusion and levels of expression of GFRa-1 and c-Ret mRNA were determined by in situ hybridization histochemistry. (ncl.edu.tw)