Bibliographies thématiques / Reperfusion injury

Littérature scientifique sur le sujet « Reperfusion injury »

Auteur : Grafiati
Publié le 4 juin 2021
Mis à jour le 10 mars 2023

Créez une référence correcte selon les styles APA, MLA, Chicago, Harvard et plusieurs autres

Choisissez une source :

Sommaire

Consultez les listes thématiques d’articles de revues, de livres, de thèses, de rapports de conférences et d’autres sources académiques sur le sujet « Reperfusion injury ».

À côté de chaque source dans la liste de références il y a un bouton « Ajouter à la bibliographie ». Cliquez sur ce bouton, et nous générerons automatiquement la référence bibliographique pour la source choisie selon votre style de citation préféré : APA, MLA, Harvard, Vancouver, Chicago, etc.

Vous pouvez aussi télécharger le texte intégral de la publication scolaire au format pdf et consulter son résumé en ligne lorsque ces informations sont inclues dans les métadonnées.

Articles de revues sur le sujet "Reperfusion injury"

1

Khalil, Alizan A., Farah A. Aziz et John C. Hall. « Reperfusion Injury ». Plastic and Reconstructive Surgery 117, no 3 (mars 2006) : 1024–33. http://dx.doi.org/10.1097/01.prs.0000204766.17127.54.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
2

Grinyo, J. M. « Reperfusion injury ». Transplantation Proceedings 29, no 1-2 (février 1997) : 59–62. http://dx.doi.org/10.1016/s0041-1345(96)00715-4.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
3

Quinones-Baldrich, William J., et Deborah Caswell. « Reperfusion Injury ». Critical Care Nursing Clinics of North America 3, no 3 (septembre 1991) : 525–34. http://dx.doi.org/10.1016/s0899-5885(18)30722-6.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
4

Royston, David. « Reperfusion injury ». Baillière's Clinical Anaesthesiology 2, no 3 (septembre 1988) : 707–27. http://dx.doi.org/10.1016/s0950-3501(88)80014-x.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
5

Zimmerman, Barbara J., et D. Neil Granger. « Reperfusion Injury ». Surgical Clinics of North America 72, no 1 (février 1992) : 65–83. http://dx.doi.org/10.1016/s0039-6109(16)45628-8.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
6

Reichek, Nathaniel, et Kambiz Parcham-Azad. « Reperfusion Injury ». Journal of the American College of Cardiology 55, no 12 (mars 2010) : 1206–8. http://dx.doi.org/10.1016/j.jacc.2009.10.048.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
7

Flaherty, John T., et Myron L. Weisfeldt. « Reperfusion injury ». Free Radical Biology and Medicine 5, no 5-6 (janvier 1988) : 409–19. http://dx.doi.org/10.1016/0891-5849(88)90115-3.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
8

Fishbein, M. C. « Reperfusion injury ». Clinical Cardiology 13, no 3 (mars 1990) : 213–17. http://dx.doi.org/10.1002/clc.4960130312.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
9

Ma, Yulong, Yanhui Cai, Doutong Yu, Yuting Qiao, Haiyun Guo, Zejun Gao et Li Guo. « Astrocytic Glycogen Mobilization in Cerebral Ischemia/Reperfusion Injury ». Neuroscience and Neurological Surgery 11, no 3 (21 février 2022) : 01–05. http://dx.doi.org/10.31579/2578-8868/228.

Texte intégral
Résumé :
Glycogen is an important energy reserve in the brain and can be rapidly degraded to maintain metabolic homeostasis during cerebral blood vessel occlusion. Recent studies have pointed out the alterations in glycogen and its underlying mechanism during reperfusion after ischemic stroke. In addition, glycogen metabolism may work as a promising therapeutic target to relieve reperfusion injury. Here, we summarize the progress of glycogen metabolism during reperfusion injury and its corresponding application in patients suffering from ischemic stroke.
Styles APA, Harvard, Vancouver, ISO, etc.
10

Bodwell, Wendy. « Ischemia, reperfusion, and reperfusion injury ». Journal of Cardiovascular Nursing 4, no 1 (novembre 1989) : 25–32. http://dx.doi.org/10.1097/00005082-198911000-00005.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
Plus de sources

Thèses sur le sujet "Reperfusion injury"

1

Mankad, Pankaj Shashikant. « Ischaemia-reperfusion injury and endothelial dysfunction ». Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392286.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
2

Amrani, Mohamed. « Postischemic coronary flow and reperfusion injury ». Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307467.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
3

Koo, Dicken D. H. « Ischaemia/reperfusion injury in renal transplantation ». Thesis, University of Oxford, 1999. http://ora.ox.ac.uk/objects/uuid:e0177fd9-1504-4c76-b9fd-6e7ae0b6b466.

Texte intégral
Résumé :
Kidney transplants from both living-related (LRD) and living unrelated (LURD) donors have superior function and survival than transplants from cadaver donors. This may be unsurprising as kidneys from living donors are procured under optimal conditions, from healthy donors with minimal ischaemia times. In contrast, cadaver kidneys are obtained from traumatised donors and may experience extended periods of cold ischaemic storage before transplantation. An immunohistochemical analysis has been performed on biopsies obtained before, and immediately after transplantation, to investigate the potential causes of early inflammatory events associated with cadaver renal transplantation that may influence subsequent graft outcome. An immunohistochemical analysis of biopsies obtained before transplantation demonstrated upregulated expression of endothelial E-selectin and proximal tubular expression of ICAM-1, VCAM-1 and HLA Class II antigens in cadaver donor kidneys. Analysis of donor parameters demonstrated that traumatic physiological events experienced in intensive care around the time of brain death were significantly associated with the induction of proinflammatory antigens. Antigen induction in cadaver donor kidneys before transplantation was significantly associated with early acute rejection. Furthermore, in cadaveric kidneys with long cold ischaemia times, glomerular neutrophil infiltration and deposition of activated platelets expressing P-selectin on intertubular capillaries were detected following reperfusion, in association with impaired short and long term graft function. Expression of inflammatory mediators were absent in all LRD renal allografts before and after reperfusion. A clinical trial was performed to determine whether ischaemia/reperfusion injury may be ameliorated by reflushing cadaver kidneys after cold storage to remove harmful products that may have accumulated in the vessel lumen. Reflushing did not prevent the inflammatory events observed after reperfusion or improve graft function. Therefore, a novel, oxygen free radical scavenger (lec-SOD) was obtained to assess its potential efficacy in preventing ischaemia/reperfusion injury. Lec-SOD bound with high affinity to macro- and microvascular endothelial cells under cold hypoxic conditions following incorporation into Marshall's preservation solution, significantly inhibiting cold hypoxia induced cell death, adhesion molecule induction and neutrophil adhesion. Furthermore, preservation of kidneys with lec- SOD for 18 hr in an experimental model of chronic renal allograft rejection, significantly attenuated neutrophil infiltration and MHC Class I induction day 1 post-transplant, with improved long term renal function. The results presented in this Thesis demonstrate that donor factors and cold ischaemia/ reperfusion injury elicit an early inflammatory response that may influence graft outcome of cadaver kidneys. Refinements in donor management and organ preservation may limit the deleterious effects of ischaemia/reperfusion injury in cadaver renal allografts, increasing graft survival to that observed in living donor transplantation.
Styles APA, Harvard, Vancouver, ISO, etc.
4

Nitisha, Hiranandani. « Impact of Reperfusion Injury on Heart ». The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1239720273.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
5

Aluri, Hema. « INTRA-MITOCHONDRIAL INJURY DURING ISCHEMIA-REPERFUSION ». VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/474.

Texte intégral
Résumé :
Cardiac injury is increased following ischemia-reperfusion. Mitochondria are the “effector organelles” that are damaged during ischemia (ISC) when there is no blood flow. Resumption of metabolism by damaged mitochondria during reperfusion (REP) results in increased cell injury. Current therapeutic interventions to pre-condition and post-condition the heart during ISC are ineffective during certain conditions like aging and diabetes due to defects in the signaling cascades. In contrast, mitochondrial-based strategies are effective in protecting the heart during ISC-REP. Hence direct therapeutic targeting of dysfunctional mitochondria will provide the potential to bypass the upstream signaling defects and intervene directly upon the effector organelle. Novel mitochondrial-targeted therapy relies on understanding the sites in the electron transport chain (ETC) that are damaged by ISC and produce cell-injury during REP. This project identifies a novel pathological role of cytochrome c in depleting cardiolipin during ischemia after which the mitochondria are in a defective condition that leads to additional cell death during reperfusion. During ischemia oxidants from complex III oxidize cytochrome c, forming a peroxidase, which causes oxidative damage and depletion of cardiolipin. Depletion of cardiolipin disrupts normal physiology and augments cell death. Identification of the innovative pathobiology during ISC-REP recognizes a novel therapeutic target, cytochrome c peroxidase, which can be a focal point for new therapeutic interventions to decrease cardiac injury. In order to maintain homeostatis, living organisms have the methionine sulfoxide reductase system, which reduce both free and protein bound Met(O) back to methionine (Met) in the presence of thioredoxin. Oxidized Trx is inactive and unable to bind to ASK1 thereby activating ASK1 and causing cell death via p38/JNK pathways thereby contributing to the pathogenesis of myocardial ISC-REP injury. In this study we have shown that inhibition of ASK1 protects the heart during REP via the modulation of mitochondria that sustained damage during ISC. The mitochondrial-based mechanism of cardioprotection with ASK1 inhibition enhanced the functional integrity of the inner mitochondrial membrane retaining cytochrome c thereby decreasing cell death. This therapeutic intervention is a key step to achieve the ultimate goal to improve clinical outcomes in patients that suffer an acute myocardial infarction.
Styles APA, Harvard, Vancouver, ISO, etc.
6

Fitridge, Robert Alwyn. « Reperfusion injury in focal cerebral ischaemia / ». Title page, table of contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09MS/09msf546.pdf.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
7

MIHAYLOV, PLAMEN VESELINOV. « Ischemic reperfusion injury in Liver transplantation ». Doctoral thesis, Università degli studi di Pavia, 2021. http://hdl.handle.net/11571/1434014.

Texte intégral
Résumé :
About 119,592 patients are currently on the organ transplant waiting list in the US, with the number increasing by 5% every year. In 2017, 11,640 candidates were added to the liver transplant waiting list. While the increase in the number of liver transplants is encouraging, the organ shortage remains critically high. During 2015, 1673 patients died without undergoing transplant and another 1227 were removed from the waiting list due to being too sick to undergo transplant. The major untapped pool of donor organs that could be used to alleviate this crisis in organ transplantation are steatotic livers and livers from Donors after Cardiac Death (DCD). Steatotic liver grafts are associated with an early allograft dysfunction rate of 60%-80% compared with less than 5% for nonsteatotic grafts. This is due to their poor tolerance to ischemic reperfusion injury. On the other hand, only 27% (518/1884) of the DCD livers were transplanted in 2017. The single major reason for this is the severe ischemia reperfusion injury in these livers. The severity of ischemic reperfusion injury is an important determinant of allograft function post-transplant. However, the mechanisms that contribute to increased susceptibility of steatotic and DCD grafts to ischemic reperfusion injury remains poorly defined. In solid organ transplantation, graft damage subsequent to ischemic reperfusion injury may result in delayed graft function. In the worst case, this complication can lead to primary graft non- function resulting in an urgent need of re-transplantation. Ischemic reperfusion injury is the consequence of temporary interruption of blood flow to the liver. Warm ischemia reperfusion injury occurs during clamping of vascular inflow during prolonged liver resections and during a donation after cardiac death organ retrieval procedure. Cold ischemia reperfusion injury results from maintenance of the liver in cold preservation and subsequent reperfusion of the graft during transplantation. Apart from its pivotal role in the pathogenesis of the liver’s post reperfusion injury, it has also been involved as an underlying mechanism responsible for the dysfunction and injury of other organs as well. Liver ischemia and reperfusion in settings of liver transplant represent an event with consequences that influence the function of many organs including the lung, kidney, intestine, pancreas, adrenals, and myocardium among others. The molecular and clinical manifestation of these remote organ injuries can ultimately lead to multiple organ dysfunction syndrome. The objective of this thesis is to give a full and comprehensive analysis of ischemic reperfusion injury in liver transplantation.
About 119,592 patients are currently on the organ transplant waiting list in the US, with the number increasing by 5% every year. In 2017, 11,640 candidates were added to the liver transplant waiting list. While the increase in the number of liver transplants is encouraging, the organ shortage remains critically high. During 2015, 1673 patients died without undergoing transplant and another 1227 were removed from the waiting list due to being too sick to undergo transplant. The major untapped pool of donor organs that could be used to alleviate this crisis in organ transplantation are steatotic livers and livers from Donors after Cardiac Death (DCD). Steatotic liver grafts are associated with an early allograft dysfunction rate of 60%-80% compared with less than 5% for nonsteatotic grafts. This is due to their poor tolerance to ischemic reperfusion injury. On the other hand, only 27% (518/1884) of the DCD livers were transplanted in 2017. The single major reason for this is the severe ischemia reperfusion injury in these livers. The severity of ischemic reperfusion injury is an important determinant of allograft function post-transplant. However, the mechanisms that contribute to increased susceptibility of steatotic and DCD grafts to ischemic reperfusion injury remains poorly defined. In solid organ transplantation, graft damage subsequent to ischemic reperfusion injury may result in delayed graft function. In the worst case, this complication can lead to primary graft non- function resulting in an urgent need of re-transplantation. Ischemic reperfusion injury is the consequence of temporary interruption of blood flow to the liver. Warm ischemia reperfusion injury occurs during clamping of vascular inflow during prolonged liver resections and during a donation after cardiac death organ retrieval procedure. Cold ischemia reperfusion injury results from maintenance of the liver in cold preservation and subsequent reperfusion of the graft during transplantation. Apart from its pivotal role in the pathogenesis of the liver’s post reperfusion injury, it has also been involved as an underlying mechanism responsible for the dysfunction and injury of other organs as well. Liver ischemia and reperfusion in settings of liver transplant represent an event with consequences that influence the function of many organs including the lung, kidney, intestine, pancreas, adrenals, and myocardium among others. The molecular and clinical manifestation of these remote organ injuries can ultimately lead to multiple organ dysfunction syndrome. The objective of this thesis is to give a full and comprehensive analysis of ischemic reperfusion injury in liver transplantation.
Styles APA, Harvard, Vancouver, ISO, etc.
8

Thummachote, Mr Yongsuk. « The pathopysiological consequence of ischaemia reperfusion injury ». Thesis, University of London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498481.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
9

Kinross, James M. « Systems metabolism of intestinal ischaemia/reperfusion injury ». Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.543342.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
10

Winbladh, Anders. « Microdialysis in Liver Ischemia and Reperfusion injury ». Doctoral thesis, Linköpings universitet, Kirurgi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-68651.

Texte intégral
Résumé :
Introduction: New chemotherapy regimens and improvements in surgical technique have increased the number of patients with liver tumours eligible for curative liver resection. There is a significant risk of bleeding during liver surgery, but this risk can be reduced if the portal inflow is temporarily closed; i.e. the Pringles maneuver (PM). If the PM is used, the liver will suffer from ischemia and reperfusion injury (IRI). If the liver remnant is too small or if the patient has chronic liver disease, the IRI may inhibit the regeneration of the liver remnant. The patient may then die from postoperative liver failure. Several strategies have been tried to protect the liver from IRI. For instance can the PM be applied in short intervals or reactive oxygen species can be scavenged by antioxidants. There are no sensitive methods available for studying IRI in patients and little is known how IRI affects the metabolism in the liver. Microdialysis is a technique that allows for continuous sampling of interstitial fluid in the organ of interest Aim: To investigate the effects of ischemia and reperfusion on glucose metabolism in the liver using the microdialysis technique. Method: A porcine model of segmental ischemia and reperfusion was developed. The hepatic perfusion and glucose metabolism was followed for 6-8 hours by placing microdialysis catheters in the liver parenchyma (studies I-III). In study IV, 16 patients were randomized to have 10 minutes of ischemic preconditioning prior to the liver resection, which was performed with 15 minutes of ischemia and 5 minutes of reperfusion repetitively until the tumour(s) were resected. Results: During ischemia the glucose metabolism was anaerobic in the ischemic segment, while the perfused segment had normal glucose metabolism. Urea was added in the perfusate of the microdialysis catheters and was found to be a reliable marker of liver perfusion. The antioxidant NAcetylcystein (NAC) improved the hepatic aerobic glucose metabolism in the pig during the reperfusion, shown as reduced levels of lactate and improved glycogenesis in the hepatocytes. This can be explained by the scavenging of nitric oxide by NAC as nitric oxide otherwise would inhibit mitochondrial respiration. Also IP improved aerobic glucose metabolism resulting in lower hepatic lactate levels in patients having major liver resections. Conclusion: Microdialysis can monitor the glucose metabolism both in animal experimental models and in patients during and after hepatectomy. Both NAC and IP improves aerobic glucose metabolism, which can be of value in patients with compromised liver function postoperatively.
Styles APA, Harvard, Vancouver, ISO, etc.
Plus de sources

Livres sur le sujet "Reperfusion injury"

1

A, Grace P., et Mathie Robert T, dir. Ischaemia reperfusion injury. Oxford : Blackwell Science, 1999.

Trouver le texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
2

1946-, Das Dipak Kumar, dir. Pathophysiology of reperfusion injury. Boca Raton : CRC Press, 1993.

Trouver le texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
3

1946-, Das Dipak Kumar, dir. Cellular, biochemical, and molecular aspects of reperfusion injury. New York : New York Academy of Sciences, 1994.

Trouver le texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
4

M, Yellon Derek, Jennings Robert B. 1926- et Council on Cardiac Metabolism, dir. Myocardial protection : The pathophysiology of reperfusion and reperfusion injury. New York : Raven Press, 1992.

Trouver le texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
5

Kaski, Juan Carlos, Derek J. Hausenloy, Bernard John Gersh et Derek M. Yellon, dir. Management of Myocardial Reperfusion Injury. London : Springer London, 2012. http://dx.doi.org/10.1007/978-1-84996-019-9.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
6

Kaski, Juan Carlos. Management of myocardial reperfusion injury. Dordrecht : Springer, 2012.

Trouver le texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
7

Takenobu, Kamada, Shiga Takeshi 1931- et McCuskey Robert S, dir. Tissue perfusion and organ fuction : Ischemia/reperfusion injury. Amsterdam, the Netherlands : Elsevier, 1996.

Trouver le texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
8

Bilenko, M. V. Ishemicheskie i reperfuzionnye povrezhdeniia organov : Molekuliarnye mekhanizmy, puti preduprezhdeniia i lecheniia. Moskva : Meditsina, 1989.

Trouver le texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
9

A, Fantini Gary, dir. Ischemia-reperfusion of skeletal muscle. Austin : R.G. Landes, 1994.

Trouver le texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
10

Tósaki, Árpád. Reperfusion-induced arrhythmias : Control and mechanisms. Budapest : Scientia Pub., 1995.

Trouver le texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
Plus de sources

Chapitres de livres sur le sujet "Reperfusion injury"

1

Reimer, K. A., et R. B. Jennings. « Reperfusion Injury ». Dans Reperfusion and Revascularization in Acute Myocardial Infarction, 52–55. Berlin, Heidelberg : Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83544-5_6.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
2

Dancygier, Henryk, et Peter Schirmacher. « Reperfusion Injury ». Dans Clinical Hepatology, 185–87. Berlin, Heidelberg : Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-93842-2_16.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
3

Guerci, A. D. « Reperfusion injury ». Dans Clinics of CSI, 63–70. Heidelberg : Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-662-11328-8_7.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
4

Pohlman, Timothy. « Reperfusion Injury ». Dans Thoracic Trauma and Critical Care, 29–42. Boston, MA : Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1127-4_4.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
5

Hobson, Michael J., et Basilia Zingarelli. « Ischemia-Reperfusion Injury ». Dans Pediatric Critical Care Medicine, 251–68. London : Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6362-6_24.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
6

Ošt’ádal, Bohuslav, et František Kolář. « Reperfusion-Induced Injury ». Dans Basic Science for the Cardiologist, 65–79. Boston, MA : Springer US, 1999. http://dx.doi.org/10.1007/978-1-4757-3025-8_3.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
7

van Wijck, Kim, et Wim A. Buurman. « Ischemia-Reperfusion Injury ». Dans Encyclopedia of Exercise Medicine in Health and Disease, 484–87. Berlin, Heidelberg : Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_268.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
8

Smith, Josh, et Robert Goggs. « Ischemia-Reperfusion Injury ». Dans Textbook of Small Animal Emergency Medicine, 1019–29. Hoboken, NJ, USA : John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119028994.ch158.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
9

Zingarelli, Basilia. « Ischemia-Reperfusion Injury ». Dans Science and Practice of Pediatric Critical Care Medicine, 1–12. London : Springer London, 2008. http://dx.doi.org/10.1007/978-1-84800-921-9_20.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
10

Pandey, Chandra Kant, S. S. Nath et Manish Tandon. « Ischemia–Reperfusion Injury ». Dans Peri-operative Anesthetic Management in Liver Transplantation, 199–208. Singapore : Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-6045-1_16.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.

Actes de conférences sur le sujet "Reperfusion injury"

1

La Barck, Anthony J., Jennifer E. Akers et Thomas L. Merrill. « Tissue Oxygen Transfer During Reperfusion and Post-Conditioning ». Dans ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53064.

Texte intégral
Résumé :
Heart disease is the leading cause of death in the United States. Ischemic heart disease occurs when coronary blood flow to the heart is reduced, limiting the amount of oxygen and nutrients the heart receives. When blood flow is restored after a percutaneous transluminal coronary intervention (PCI), rapid reperfusion from sudden balloon deflation can cause further injury to oxygen-starved tissue, leading to increased cell injury and cell death. Studies in animal models with ischemic heart disease have shown that reperfusion injury may account for up to 50% of the final infarct size [1]. Post-conditioning (PC) may reduce the amount of reperfusion injury by applying intermittent periods of ischemia during the early moments of reperfusion. This procedure periodically occludes blood vessels during reperfusion by periodically inflating and deflating an angioplasty balloon according to a specific algorithm. Zhao et al. showed that PC reduced reperfusion injury in a canine model by applying 3 cycles of 30 seconds of reperfusion followed by 30 seconds of ischemia (re-occlusion) at the onset of reperfusion. PC in this study reduced tissue AN/AAR (area of necrosis/area at risk) by 48% [2]. In 2008, Gao et al. demonstrated that the effectiveness of PC in rats was dependent on the number of cycles in the PC algorithm, as well as the durations of the ischemia/reperfusion phases [3].
Styles APA, Harvard, Vancouver, ISO, etc.
2

Akers, Jennifer E., Denise R. Merrill, Todd J. Nilsen, Kevin J. Koomalsingh, Masahito Minakawa, Takashi Shuto, Joseph H. Gorman, Robert C. Gorman, Matthew J. Gillespie et Thomas L. Merrill. « Localized Cooling Device for Myocardial Tissue Salvage ». Dans ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53155.

Texte intégral
Résumé :
The primary goal in treating heart attack is to restore blood flow to blocked areas of the heart. However, even after blood flow is restored, injury can occur as a result of a complex cascade of mechanisms following the reintroduction of flow, aptly referred to as reperfusion injury. Studies show that reperfusion injury is accountable for up to 50% of cell death following an ischemic period [1]. Adjunctive therapies are needed to reduce reperfusion injury.
Styles APA, Harvard, Vancouver, ISO, etc.
3

Kasparian, S., D. Gotur, S. H. L. Hsu et J. Zimmerman. « Reperfusion Injury with Resolving Saddle Pulmonary Embolism ». Dans American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1783.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
4

Merrill, Thomas L., Denise R. Merrill et Jennifer E. Akers. « Localized Brain Tissue Cooling for Use During Intracranial Thrombectomy ». Dans ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80083.

Texte intégral
Résumé :
The primary goal of current ischemic stroke treatment is quickly restoring blood perfusion. Recanalization is linked to improved neurological outcomes [1]. Resulting tissue necrosis, however, following a stroke has two causes: 1) ischemic injury and 2) reperfusion injury. Therefore, development of neuroprotective agents specifically beneficial against reperfusion injury are required.
Styles APA, Harvard, Vancouver, ISO, etc.
5

Iribarren, Juan B., et Harish Seethamraju. « Reperfusion Injury Post Lung Transplant- A Reversible Cause ». Dans American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5397.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
6

Sayah, David M., Fengchun Liu, Axelle Caudrillier et Mark R. Looney. « Neutrophil Extracellular Traps In Ischemia-Reperfusion Lung Injury ». Dans American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5123.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
7

Park, H. K. « Wavelet Analysis of Ischemia and Reperfusion Injury Models ». Dans 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1616862.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
8

Bhandal, J., A. Hussain, J. Buckley et H. Maddock. « P34 Adenosine a1 receptor activation can protect the myocardium from ischaemia reperfusion injury post reperfusion ». Dans British Society for Cardiovascular Research, Autumn Meeting 2017 ‘Cardiac Metabolic Disorders and Mitochondrial Dysfunction’, 11–12 September 2017, University of Oxford. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bscr.39.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
9

Xia, Cao, Ma Kewei, Liu Yicheng, Yu Xiaofeng, Chen Yanping, Sui Dayuan, Pei Jin et Gu Xinquan. « Effects of Ginsenoside Re on myocardial ischemia reperfusion injury ». Dans 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027905.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
10

De Almeida, Francine Maria, Angela da Silva Battochio, João Vitor Pithon Napoli, Katiusa Abreu Alves, Manoel Carneiro de Oliveira-Junior, Henrique Takachi Moriya, Paulo Manuel Pêgo-Fernandes, Rodolfo de Paula Vieira, Rogerio Pazetti et Grace Balbin Silva. « Creatine supplementation attenuates ischemia-reperfusion injury in lung transplantation ». Dans ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1545.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.

Rapports d'organisations sur le sujet "Reperfusion injury"

1

Omaye, Stanley T. Efficacy of Gamma-glutamylcysteine (GGC) in Ischemia-reperfusion Injury. Fort Belvoir, VA : Defense Technical Information Center, octobre 2012. http://dx.doi.org/10.21236/ada568392.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
2

Omaye, Stanley T. Efficacy of Gamma-glutamylcysteine (GGC) in Ischemia-reperfusion Injury. Fort Belvoir, VA : Defense Technical Information Center, juillet 2012. http://dx.doi.org/10.21236/ada579994.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
3

Zheng, Jinghui. Quercetin for Myocardial Ischemia/Reperfusion Injury : A Preclinical Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review Protocols, avril 2020. http://dx.doi.org/10.37766/inplasy2020.4.0162.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
4

Lu, Liying, Xiaocong Ma, Jinghui Zheng, Lijuan Li, Wenna Yang, Yixuan Kong et Jie Wang. Quercetin for Myocardial Ischemia Reperfusion Injury : A Protocol for Systematic Review and Meta Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, mai 2020. http://dx.doi.org/10.37766/inplasy2020.5.0067.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
5

Percival, Thomas J., Shimul Patel, Nickolay P. Markov, Jerry R. Spencer, Gabriel E. Burkhardt et Todd E. Rasmussen. The Impact of Prophylactic Fasciotomy Following Porcine (Sus scrofa) Hind Limb Ischemia/Reperfusion Injury. Fort Belvoir, VA : Defense Technical Information Center, mars 2012. http://dx.doi.org/10.21236/ada559521.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
6

Wu, Lihua, Ling Wu, Yu Liu, Ting Jiang, Ju Yang et Mingquan Li. Can resveratrol protect against renal ischemia/reperfusion injury ? A systematic review and meta-analysis of preclinical studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, avril 2021. http://dx.doi.org/10.37766/inplasy2021.4.0102.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
7

Yu, Beibei, Yongfeng Zhang et Shouping Gong. Effects of miRNA-modified exosomes alleviate cerebral ischemic reperfusion injury in Pre-clinical Studies : A Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, mai 2022. http://dx.doi.org/10.37766/inplasy2022.5.0062.

Texte intégral
Résumé :
Review question / Objective: The purpose of this study was to investigate the effect of miRNA-modified exosomes in alleviating cerebral ischemic reperfusion injury compared with the non-treatment group. The research object is an animal model of middle cerebral artery occlusion. The research method is a controlled study. The primary outcome of this study was infarct volume, and the secondary outcome was neurobehavioral performance. Main outcome(s): The primary outcome of this study was Infarct volumes，which was measured by 2,3,5-triphenyltetranzolium chloride (TTC) staining. And it was calculated as followed: Infarct volume % = lesion area of each section = (contralateral hemisphere area/ipsilateral hemisphere area) × ipsilateral lesion area. Neurobehavioral performance was the secondary outcome, and was assessed by three scoring scales: modified neurological severity score (mNSS), Longa scoring system and neurological deficit score (NDS).
Styles APA, Harvard, Vancouver, ISO, etc.
8

Percival, Thomas J., Shimul Patel, Nickolay P. Markov, Jerry R. Spencer, Gabriel E. Burkhardt, Lorne H. Blackbourne et Todd E. Rasmussen. Fasciotomy Reduces Compartment Pressures and Improves Recovery in a Porcine Model of Extremity Vascular Injury and Ischemia/Reperfusion. Fort Belvoir, VA : Defense Technical Information Center, octobre 2012. http://dx.doi.org/10.21236/ada568830.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
9

He, Miao, Sen Wang, Jing You, Jing Shi, Yanbing Yin et Weirong Li. Neuroprotective effects of resveratrol against cerebral ischemia/reperfusion injury through anti-oxidant and anti-inflammatory mechanisms：A Systematic Review and Meta-Analysis in Rodents. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, août 2022. http://dx.doi.org/10.37766/inplasy2022.8.0059.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
10

Bowman, Phillip. Amelioration of Ischemia/Reperfusion Injury During Resuscitation from Hemorrhage by Induction of Heme Oxygenase-1 (HO-1) in a Conscious Mouse Model of Uncontrolled Hemorrhage. Fort Belvoir, VA : Defense Technical Information Center, septembre 2011. http://dx.doi.org/10.21236/ada602332.

Texte intégral
Styles APA, Harvard, Vancouver, ISO, etc.
Vous pouvez également être intéressé par les bibliographies sur le sujet « Reperfusion injury » pour d’autres types de sources :
Articles de revues Thèses Livres
Nous offrons des réductions sur tous les plans premium pour les auteurs dont les œuvres sont incluses dans des sélections littéraires thématiques. Contactez-nous pour obtenir un code promo unique!

Vers la bibliographie