Se connecter

Bibliographies thématiques / Reperfusion injury / Articles de revues

Articles de revues sur le sujet « Reperfusion injury »

Pour voir les autres types de publications sur ce sujet consultez le lien suivant : 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 :

Consultez les 50 meilleurs articles de revues pour votre recherche 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.

Parcourez les articles de revues sur diverses disciplines et organisez correctement votre bibliographie.

1

Khalil, Alizan A., Farah A. Aziz et John C. Hall. « Reperfusion Injury ». Plastic and Reconstructive Surgery 117, n^o 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, n^o 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, n^o 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, n^o 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, n^o 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, n^o 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, n^o 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, n^o 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, n^o 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, n^o 1 (novembre 1989) : 25–32. http://dx.doi.org/10.1097/00005082-198911000-00005.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

11

Songur, Çetin Murat. « Ischemia-Reperfusion Injury ». Kosuyolu Heart Journal 18, n^o 2 (3 août 2015) : 89–93. http://dx.doi.org/10.5578/khj.5774.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

12

Yellon, Derek M., et Derek J. Hausenloy. « Myocardial Reperfusion Injury ». New England Journal of Medicine 357, n^o 11 (13 septembre 2007) : 1121–35. http://dx.doi.org/10.1056/nejmra071667.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

13

Souidi, Naima, Meaghan Stolk et Martina Seifert. « Ischemia–reperfusion injury ». Current Opinion in Organ Transplantation 18, n^o 1 (février 2013) : 34–43. http://dx.doi.org/10.1097/mot.0b013e32835c2a05.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

14

Misinski, Maureen. « Myocardial Reperfusion Injury ». Critical Care Nursing Clinics of North America 2, n^o 4 (décembre 1990) : 651–62. http://dx.doi.org/10.1016/s0899-5885(18)30785-8.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

15

AMBROSIO, G. « Myocardial reperfusion injury ». European Heart Journal Supplements 4 (mars 2002) : B28—B30. http://dx.doi.org/10.1016/s1520-765x(02)90013-1.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

16

Ko, Wilson, Arthur S. Hawes, W. Douglas Lazenby, Steven E. Calvano, Yong T. Shin, John A. Zelano, Anthony C. Antonacci, O. Wayne Isom et Karl H. Krieger. « Myocardial reperfusion injury ». Journal of Thoracic and Cardiovascular Surgery 102, n^o 2 (août 1991) : 297–308. http://dx.doi.org/10.1016/s0022-5223(19)36563-8.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

17

Huber, Thomas. « Ischaemia-reperfusion injury ». Journal of Vascular Surgery 31, n^o 5 (mai 2000) : 1081–82. http://dx.doi.org/10.1067/mva.2000.105513.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

18

Boyle, Edward M., Timothy H. Pohlman, Carol J. Cornejo et Edward D. Verrier. « Ischemia-Reperfusion Injury ». Annals of Thoracic Surgery 64, n^o 4 (octobre 1997) : S24—S30. http://dx.doi.org/10.1016/s0003-4975(97)00958-2.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

19

Olds, Robin. « Ischaemia–reperfusion injury ». Pathology 31, n^o 4 (1999) : 444. http://dx.doi.org/10.1016/s0031-3025(16)34766-3.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

20

Tilney, N. L., D. Paz, J. Ames, M. Gasser, I. Laskowski et W. W. Hancock. « Ischemia-reperfusion injury ». Transplantation Proceedings 33, n^o 1-2 (février 2001) : 843–44. http://dx.doi.org/10.1016/s0041-1345(00)02341-1.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

21

Dorweiler, Bernhard, Diethard Pruefer, Terezia B. Andrasi, Sasa M. Maksan, Walther Schmiedt, Achim Neufang et Christian F. Vahl. « Ischemia-Reperfusion Injury ». European Journal of Trauma and Emergency Surgery 33, n^o 6 (20 novembre 2007) : 600–612. http://dx.doi.org/10.1007/s00068-007-7152-z.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

22

McIntyre, Kenneth E. « ISCHAEMIA-REPERFUSION INJURY ». Shock 12, n^o 3 (septembre 1999) : 246. http://dx.doi.org/10.1097/00024382-199909000-00019.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

23

AL-QATTAN, M. M. « Ischaemia-Reperfusion Injury ». Journal of Hand Surgery 23, n^o 5 (octobre 1998) : 570–73. http://dx.doi.org/10.1016/s0266-7681(98)80003-x.

Texte intégral

Résumé :

Prolonged ischaemia sometimes occurs in replantation and free flap surgery. The re-establishment of circulatory flow to the ischaemic tissue leads to a cascade of events which augments tissue necrosis. This paper reviews the pathophysiology of this ischaemia-reperfusion injury and discusses different methods to modulate this injury.

Styles APA, Harvard, Vancouver, ISO, etc.

24

YAMAZAKI, NOBORU. « Myocardial reperfusion injury. » Nihon Naika Gakkai Zasshi 81, n^o 7 (1992) : 1119–24. http://dx.doi.org/10.2169/naika.81.1119.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

25

Widgerow, Alan D. « Ischemia-Reperfusion Injury ». Annals of Plastic Surgery 72, n^o 2 (février 2014) : 253–60. http://dx.doi.org/10.1097/sap.0b013e31825c089c.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

26

Grace, P. A. « Ischaemia-reperfusion injury ». British Journal of Surgery 81, n^o 5 (mai 1994) : 637–47. http://dx.doi.org/10.1002/bjs.1800810504.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

27

Anaya-Prado, Roberto, Luis H. Toledo-Pereyra, Alex B. Lentsch et Peter A. Ward. « Ischemia/Reperfusion Injury ». Journal of Surgical Research 105, n^o 2 (juin 2002) : 248–58. http://dx.doi.org/10.1006/jsre.2002.6385.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

28

Geng, Xiaokun, Jie Gao, Alexandra Wehbe, Fengwu Li, Naveed Chaudhry, Changya Peng et Yuchuan Ding. « Reperfusion and reperfusion injury after ischemic stroke ». Environmental Disease 7, n^o 2 (2022) : 33. http://dx.doi.org/10.4103/ed.ed_12_22.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

29

GARCIADORADO, D., et H. PIPER. « Postconditioning : Reperfusion of “reperfusion injury” after hibernation ». Cardiovascular Research 69, n^o 1 (janvier 2006) : 1–3. http://dx.doi.org/10.1016/j.cardiores.2005.11.011.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

30

Kang, K. J. « Mechanism of hepatic ischemia/reperfusion injury and protection against reperfusion injury ». Transplantation Proceedings 34, n^o 7 (novembre 2002) : 2659–61. http://dx.doi.org/10.1016/s0041-1345(02)03465-6.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

31

Karmazyn, Morris. « The 1990 Merck Frosst Award. Ischemic and reperfusion injury in the heart. Cellular mechanisms and pharmacological interventions ». Canadian Journal of Physiology and Pharmacology 69, n^o 6 (1 juin 1991) : 719–30. http://dx.doi.org/10.1139/y91-108.

Texte intégral

Résumé :

Reperfusion in the heart represents an important form of tissue injury, particularly in view of the emerging importance of reperfusion protocols aimed at salvaging the ischemic myocardium. Both the manifestations and the causes of reperfusion injury are multifold. With respect to the former, reperfusion injury can be characterized by various abnormalities including development of arrhythmias, contractile dysfunction, ultrastructural damage as well as various defects in intracellular biochemical homeostasis. The mechanisms underlying myocardial reperfusion injury are equally complex, but most likely involve numerous processes acting in concert resulting in eventual cell death. In this review, a description of various such potential mechanisms, which represent primary interests of the author, are presented. An understanding of these mechanisms has led to novel pharmacological approaches towards the protection of the reperfused myocardium. For instance, several lines of evidence implicate enhanced eicosanoid, and in particular prostaglandin, synthesis in reperfusion injury, since (1) such injury is involved with enhanced prostaglandin biosynthesis, (2) inhibition of prostaglandin synthesis with various nonsteroidal anti-inflammatory drugs attenuates injury, and (3) exogenous prostaglandins increase injury. Another intracellular process that is emerging as an important contributor to reperfusion injury in the heart is the Na+/H+ exchanger, which is most likely activated upon reperfusion. Such activation would lead to numerous intracellular disturbances including the increased synthesis of prostaglandins and elevated intracellular Ca2+ concentrations. Indeed, inhibitors of Na+/H+ exchange such as amiloride have been shown to effectively inhibit reperfusion injury. Reperfusion is also associated with depressed mitochondrial function, particularly in subsarcolemmal mitochondria which are rapidly injured as a result of both ischemic and reperfusion conditions. Preservation of mitochondrial function with dissimilar approaches such as carnitine or phosphatidylcholine administration markedly reduces reperfusion injury. A nonpharmacological novel approach towards the protection of the reperfused myocardium represents the induction of so-called stress or heart shock proteins in the heart prior to initiation of ischemia and reperfusion. The salutary effect of the heat shock response may be dependent not on the heat shock proteins themselves, but through the concomitant elevation of tissue catalase content resulting in enhanced detoxification of intracellular hydrogen peroxide. Thus reperfusion injury represents numerous complex events such that manipulations aimed at limiting such injury can be initiated to prevent specific defects with the ultimate goal of an overall reduction in cell damage.Key words: heart, ischemia, reperfusion, prostaglandins, leukotrienes, Na+/H+ exchange, subsarcolemmal mitochondria, interfibrillar mitochondria, heat shock proteins, tissue protection.

Styles APA, Harvard, Vancouver, ISO, etc.

32

Sakuma, Tsutomu, Keiji Takahashi, Nobuo Ohya, Osamu Kajikawa, Thomas R. Martin, Kurt H. Albertine et Michael A. Matthay. « Ischemia-reperfusion lung injury in rabbits : mechanisms of injury and protection ». American Journal of Physiology-Lung Cellular and Molecular Physiology 276, n^o 1 (1 janvier 1999) : L137—L145. http://dx.doi.org/10.1152/ajplung.1999.276.1.l137.

Texte intégral

Résumé :

To study the mechanisms responsible for ischemia-reperfusion lung injury, we developed an anesthetized rabbit model in which the effects of lung deflation, lung inflation, alveolar gas composition, hypothermia, and neutrophils on reperfusion pulmonary edema could be studied. Rabbits were anesthetized and ventilated, and the left pulmonary hilum was clamped for either 2 or 4 h. Next, the left lung was reperfused and ventilated with 100% oxygen. As indexes of lung injury, we measured arterial oxygenation, extravascular lung water, and the influx of a vascular protein (131I-labeled albumin) into the extravascular space of the lungs. The principal results were that 1) all rabbits with the deflation of the lung during ischemia for 4 h died of fulminant pulmonary edema within 1 h of reperfusion; 2) inflation of the ischemic lung with either 100% oxygen, air, or 100% nitrogen prevented the reperfusion lung injury; 3) hypothermia at 6–8°C also prevented the reperfusion lung injury; 4) although circulating neutrophils declined during reperfusion lung injury, there was no increase in interleukin-8 levels in the plasma or the pulmonary edema fluid, and, furthermore, neutrophil depletion did not prevent the reperfusion injury; and 5) ultrastructural studies demonstrated injury to both the lung endothelium and the alveolar epithelium after reperfusion in deflated lungs, whereas the inflated lungs had no detectable injury. In summary, ischemia-reperfusion injury to the rabbit lung can be prevented by either hypothermia or lung inflation with either air, oxygen, or nitrogen.

Styles APA, Harvard, Vancouver, ISO, etc.

33

Linas, S. L., P. F. Shanley, D. Whittenburg, E. Berger et J. E. Repine. « Neutrophils accentuate ischemia-reperfusion injury in isolated perfused rat kidneys ». American Journal of Physiology-Renal Physiology 255, n^o 4 (1 octobre 1988) : F728—F735. http://dx.doi.org/10.1152/ajprenal.1988.255.4.f728.

Texte intégral

Résumé :

The contribution of neutrophils to reperfusion injury after ischemia is not known. To determine the effect of neutrophils on the function of ischemic kidneys, we added purified human neutrophils during perfusion of isolated ischemic or nonischemic rat kidneys. Reperfusion of ischemic kidneys with neutrophils caused a distinct morphological lesion of vascular endothelial and smooth muscle cells and more functional injury than reperfusion with buffered albumin alone; with neutrophils, glomerular filtration rate (GFR) was 113 +/- 7 microliter.min-1.g-1, tubular sodium reabsorption (TNa) was 72 +/- 2%; without neutrophils, GFR was 222 +/- 18 microliter.min-1.g-1; TNa was 90 +/- 2%; both P less than 0.01 vs. reperfusion with neutrophils. In contrast, addition of neutrophils did not injure control kidneys, unless the neutrophil activator, phorbol myristate acetate, was also added. Two experiments suggested that O2 metabolites contributed to neutrophil-mediated injury to ischemic kidneys. First, reperfusion of ischemic kidneys with O2 metabolite-deficient neutrophils from a patient with chronic granulomatous disease did not cause more injury than reperfusion with buffered albumin alone. Second, simultaneous addition of the O2 metabolite scavenger, catalase, prevented the GFR and TNa decreases caused by neutrophils but did not decrease injury in the absence of neutrophils. We conclude that neutrophils by an O2 metabolite-dependent mechanism contribute to ischemia-reperfusion injury in the isolated perfused kidney.

Styles APA, Harvard, Vancouver, ISO, etc.

34

Rubin, B. B., S. Liauw, J. Tittley, A. D. Romaschin et P. M. Walker. « Prolonged adenine nucleotide resynthesis and reperfusion injury in postischemic skeletal muscle ». American Journal of Physiology-Heart and Circulatory Physiology 262, n^o 5 (1 mai 1992) : H1538—H1547. http://dx.doi.org/10.1152/ajpheart.1992.262.5.h1538.

Texte intégral

Résumé :

Skeletal muscle ischemia results in energy depletion and intracellular acidosis. Reperfusion is associated with impaired adenine nucleotide resynthesis, edema formation, and myocyte necrosis. The purpose of these studies was to define the time course of cellular injury and adenine nucleotide depletion and resynthesis in postischemic skeletal muscle during prolonged reperfusion in vivo. The isolated canine gracilis muscle model was used. After 5 h of ischemia, muscles were reperfused for either 1 or 48 h. Lactate and creatine phosphokinase (CPK) release during reperfusion was calculated from arteriovenous differences and blood flow. Adenine nucleotides, nucleosides, bases, and creatine phosphate were quantified by high-performance liquid chromatography, and muscle necrosis was assessed by nitroblue tetrazolium staining. Reperfusion resulted in a rapid release of lactate, which paralleled the increase in blood flow, and a delayed but prolonged release of CPK. Edema formation and muscle necrosis increased between 1 and 48 h of reperfusion (P less than 0.05). Recovery of energy stores during reperfusion was related to the extent of postischemic necrosis, which correlated with the extent of nucleotide dephosphorylation during ischemia (r = 0.88, P less than 0.001). These results suggest that both adenine nucleotide resynthesis and myocyte necrosis, which are protracted processes in reperfusing skeletal muscle, are related to the extent of nucleotide dephosphorylation during ischemia.

Styles APA, Harvard, Vancouver, ISO, etc.

35

Goldfarb, R. D., et A. Singh. « GSH and reperfusion injury. » Circulation 80, n^o 3 (septembre 1989) : 712–13. http://dx.doi.org/10.1161/circ.80.3.2766517.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

36

Mitsos, S. E., J. C. Fantone, K. P. Gallagher, K. M. Walden, P. J. Simpson, G. D. Abrams, M. A. Schork et B. R. Lucchesi. « Canine Myocardial Reperfusion Injury ». Journal of Cardiovascular Pharmacology 8, n^o 5 (septembre 1986) : 978–88. http://dx.doi.org/10.1097/00005344-198609000-00015.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

37

Opie, Lionel H. « Mechanisms of reperfusion injury ». Current Opinion in Cardiology 6, n^o 6 (décembre 1991) : 864–67. http://dx.doi.org/10.1097/00001573-199112000-00002.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

38

Ostadal, Petr. « What is ‘reperfusion injury’ ? » European Heart Journal 26, n^o 1 (30 novembre 2004) : 99. http://dx.doi.org/10.1093/eurheartj/ehi029.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

39

Tosaki, Arpad, Anne Hellegouarch et Pierre Braquel. « Cicletanine and Reperfusion Injury ». Journal of Cardiovascular Pharmacology 17, n^o 4 (avril 1991) : 551–59. http://dx.doi.org/10.1097/00005344-199104000-00005.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

40

Weight, S. C., P. R. F. Bell et M. L. Nicholson. « Renal ischaemia-reperfusion injury ». British Journal of Surgery 83, n^o 2 (février 1996) : 162–70. http://dx.doi.org/10.1046/j.1365-2168.1996.02182.x.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

41

Rushing, G. D., et L. D. Britt. « Reperfusion Injury After Hemorrhage ». Annals of Surgery 247, n^o 6 (juin 2008) : 929–37. http://dx.doi.org/10.1097/sla.0b013e31816757f7.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

42

Clark, W. M. « Cytokines and reperfusion injury ». Neurology 49, Issue 5, Supplement 4 (1 novembre 1997) : S10—S14. http://dx.doi.org/10.1212/wnl.49.5_suppl_4.s10.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

43

Obermaier, Robert, Oliver Drognitz, Stefan Benz, Ulrich T. Hopt et Przemyslaw Pisarski. « Pancreatic Ischemia/Reperfusion Injury ». Pancreas 37, n^o 3 (octobre 2008) : 328–32. http://dx.doi.org/10.1097/mpa.0b013e31816d9283.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

44

Nosé, Peter S. « Cytokines and Reperfusion Injury ». Journal of Cardiac Surgery 8, S2 (mars 1993) : 305–8. http://dx.doi.org/10.1111/j.1540-8191.1993.tb01329.x.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

45

Frank, Anja, Megan Bonney, Stephanie Bonney, Lindsay Weitzel, Michael Koeppen et Tobias Eckle. « Myocardial Ischemia Reperfusion Injury ». Seminars in Cardiothoracic and Vascular Anesthesia 16, n^o 3 (23 février 2012) : 123–32. http://dx.doi.org/10.1177/1089253211436350.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

46

Weyker, Paul D., Christopher A. J. Webb, David Kiamanesh et Brigid C. Flynn. « Lung Ischemia Reperfusion Injury ». Seminars in Cardiothoracic and Vascular Anesthesia 17, n^o 1 (5 octobre 2012) : 28–43. http://dx.doi.org/10.1177/1089253212458329.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

47

Bascom, John U., Peter Gosling et Bashir A. Zikria. « Hepatic ischemia-reperfusion injury ». American Journal of Surgery 184, n^o 1 (juillet 2002) : 84. http://dx.doi.org/10.1016/s0002-9610(01)00838-8.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

48

Soler-Soler, J. « Trimetazidine and reperfusion injury ». European Heart Journal 22, n^o 11 (1 juin 2001) : 975. http://dx.doi.org/10.1053/euhj.2000.2529.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

49

Serracino-Inglott, Ferdinand, Nagy A. Habib et Robert T. Mathie. « Hepatic ischemia-reperfusion injury ». American Journal of Surgery 181, n^o 2 (février 2001) : 160–66. http://dx.doi.org/10.1016/s0002-9610(00)00573-0.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

50

Toledo-Pereyra, L. H. « Liver transplantation reperfusion injury ». Klinische Wochenschrift 69, n^o 21-23 (décembre 1991) : 1099–104. http://dx.doi.org/10.1007/bf01645165.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

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!