Thematische Bibliographien / Reperfusion injury / Zeitschriftenartikel
Um die anderen Arten von Veröffentlichungen zu diesem Thema anzuzeigen, folgen Sie diesem Link: Reperfusion injury.

Zeitschriftenartikel zum Thema „Reperfusion injury“

Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 31. Juli 2024

Geben Sie eine Quelle nach APA, MLA, Chicago, Harvard und anderen Zitierweisen an

Wählen Sie eine Art der Quelle aus:

Machen Sie sich mit Top-50 Zeitschriftenartikel für die Forschung zum Thema "Reperfusion injury" bekannt.

Neben jedem Werk im Literaturverzeichnis ist die Option "Zur Bibliographie hinzufügen" verfügbar. Nutzen Sie sie, wird Ihre bibliographische Angabe des gewählten Werkes nach der nötigen Zitierweise (APA, MLA, Harvard, Chicago, Vancouver usw.) automatisch gestaltet.

Sie können auch den vollen Text der wissenschaftlichen Publikation im PDF-Format herunterladen und eine Online-Annotation der Arbeit lesen, wenn die relevanten Parameter in den Metadaten verfügbar sind.

Sehen Sie die Zeitschriftenartikel für verschiedene Spezialgebieten durch und erstellen Sie Ihre Bibliographie auf korrekte Weise.

1

Khalil, Alizan A., Farah A. Aziz und John C. Hall. „Reperfusion Injury“. Plastic and Reconstructive Surgery 117, Nr. 3 (März 2006): 1024–33. http://dx.doi.org/10.1097/01.prs.0000204766.17127.54.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
2

Grinyo, J. M. „Reperfusion injury“. Transplantation Proceedings 29, Nr. 1-2 (Februar 1997): 59–62. http://dx.doi.org/10.1016/s0041-1345(96)00715-4.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
3

Quinones-Baldrich, William J., und Deborah Caswell. „Reperfusion Injury“. Critical Care Nursing Clinics of North America 3, Nr. 3 (September 1991): 525–34. http://dx.doi.org/10.1016/s0899-5885(18)30722-6.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
4

Royston, David. „Reperfusion injury“. Baillière's Clinical Anaesthesiology 2, Nr. 3 (September 1988): 707–27. http://dx.doi.org/10.1016/s0950-3501(88)80014-x.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
5

Zimmerman, Barbara J., und D. Neil Granger. „Reperfusion Injury“. Surgical Clinics of North America 72, Nr. 1 (Februar 1992): 65–83. http://dx.doi.org/10.1016/s0039-6109(16)45628-8.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
6

Reichek, Nathaniel, und Kambiz Parcham-Azad. „Reperfusion Injury“. Journal of the American College of Cardiology 55, Nr. 12 (März 2010): 1206–8. http://dx.doi.org/10.1016/j.jacc.2009.10.048.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
7

Flaherty, John T., und Myron L. Weisfeldt. „Reperfusion injury“. Free Radical Biology and Medicine 5, Nr. 5-6 (Januar 1988): 409–19. http://dx.doi.org/10.1016/0891-5849(88)90115-3.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
8

Fishbein, M. C. „Reperfusion injury“. Clinical Cardiology 13, Nr. 3 (März 1990): 213–17. http://dx.doi.org/10.1002/clc.4960130312.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
9

Ma, Yulong, Yanhui Cai, Doutong Yu, Yuting Qiao, Haiyun Guo, Zejun Gao und Li Guo. „Astrocytic Glycogen Mobilization in Cerebral Ischemia/Reperfusion Injury“. Neuroscience and Neurological Surgery 11, Nr. 3 (21.02.2022): 01–05. http://dx.doi.org/10.31579/2578-8868/228.

Der volle Inhalt der Quelle
Annotation:
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.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
10

Bodwell, Wendy. „Ischemia, reperfusion, and reperfusion injury“. Journal of Cardiovascular Nursing 4, Nr. 1 (November 1989): 25–32. http://dx.doi.org/10.1097/00005082-198911000-00005.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
11

Songur, Çetin Murat. „Ischemia-Reperfusion Injury“. Kosuyolu Heart Journal 18, Nr. 2 (03.08.2015): 89–93. http://dx.doi.org/10.5578/khj.5774.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
12

Yellon, Derek M., und Derek J. Hausenloy. „Myocardial Reperfusion Injury“. New England Journal of Medicine 357, Nr. 11 (13.09.2007): 1121–35. http://dx.doi.org/10.1056/nejmra071667.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
13

Souidi, Naima, Meaghan Stolk und Martina Seifert. „Ischemia–reperfusion injury“. Current Opinion in Organ Transplantation 18, Nr. 1 (Februar 2013): 34–43. http://dx.doi.org/10.1097/mot.0b013e32835c2a05.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
14

Misinski, Maureen. „Myocardial Reperfusion Injury“. Critical Care Nursing Clinics of North America 2, Nr. 4 (Dezember 1990): 651–62. http://dx.doi.org/10.1016/s0899-5885(18)30785-8.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
15

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

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
16

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

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
17

Huber, Thomas. „Ischaemia-reperfusion injury“. Journal of Vascular Surgery 31, Nr. 5 (Mai 2000): 1081–82. http://dx.doi.org/10.1067/mva.2000.105513.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
18

Boyle, Edward M., Timothy H. Pohlman, Carol J. Cornejo und Edward D. Verrier. „Ischemia-Reperfusion Injury“. Annals of Thoracic Surgery 64, Nr. 4 (Oktober 1997): S24—S30. http://dx.doi.org/10.1016/s0003-4975(97)00958-2.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
19

Olds, Robin. „Ischaemia–reperfusion injury“. Pathology 31, Nr. 4 (1999): 444. http://dx.doi.org/10.1016/s0031-3025(16)34766-3.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
20

Tilney, N. L., D. Paz, J. Ames, M. Gasser, I. Laskowski und W. W. Hancock. „Ischemia-reperfusion injury“. Transplantation Proceedings 33, Nr. 1-2 (Februar 2001): 843–44. http://dx.doi.org/10.1016/s0041-1345(00)02341-1.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
21

Dorweiler, Bernhard, Diethard Pruefer, Terezia B. Andrasi, Sasa M. Maksan, Walther Schmiedt, Achim Neufang und Christian F. Vahl. „Ischemia-Reperfusion Injury“. European Journal of Trauma and Emergency Surgery 33, Nr. 6 (20.11.2007): 600–612. http://dx.doi.org/10.1007/s00068-007-7152-z.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
22

McIntyre, Kenneth E. „ISCHAEMIA-REPERFUSION INJURY“. Shock 12, Nr. 3 (September 1999): 246. http://dx.doi.org/10.1097/00024382-199909000-00019.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
23

AL-QATTAN, M. M. „Ischaemia-Reperfusion Injury“. Journal of Hand Surgery 23, Nr. 5 (Oktober 1998): 570–73. http://dx.doi.org/10.1016/s0266-7681(98)80003-x.

Der volle Inhalt der Quelle
Annotation:
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.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
24

YAMAZAKI, NOBORU. „Myocardial reperfusion injury.“ Nihon Naika Gakkai Zasshi 81, Nr. 7 (1992): 1119–24. http://dx.doi.org/10.2169/naika.81.1119.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
25

Widgerow, Alan D. „Ischemia-Reperfusion Injury“. Annals of Plastic Surgery 72, Nr. 2 (Februar 2014): 253–60. http://dx.doi.org/10.1097/sap.0b013e31825c089c.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
26

Grace, P. A. „Ischaemia-reperfusion injury“. British Journal of Surgery 81, Nr. 5 (Mai 1994): 637–47. http://dx.doi.org/10.1002/bjs.1800810504.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
27

Anaya-Prado, Roberto, Luis H. Toledo-Pereyra, Alex B. Lentsch und Peter A. Ward. „Ischemia/Reperfusion Injury“. Journal of Surgical Research 105, Nr. 2 (Juni 2002): 248–58. http://dx.doi.org/10.1006/jsre.2002.6385.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
28

Pizarro, Gonzalo. „Ischemia Reperfusion Injury“. JACC: Basic to Translational Science 8, Nr. 10 (Oktober 2023): 1295–97. http://dx.doi.org/10.1016/j.jacbts.2023.08.009.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
29

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, Nr. 6 (01.06.1991): 719–30. http://dx.doi.org/10.1139/y91-108.

Der volle Inhalt der Quelle
Annotation:
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.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
30

Linas, S. L., P. F. Shanley, D. Whittenburg, E. Berger und J. E. Repine. „Neutrophils accentuate ischemia-reperfusion injury in isolated perfused rat kidneys“. American Journal of Physiology-Renal Physiology 255, Nr. 4 (01.10.1988): F728—F735. http://dx.doi.org/10.1152/ajprenal.1988.255.4.f728.

Der volle Inhalt der Quelle
Annotation:
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.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
31

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

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
32

GARCIADORADO, D., und H. PIPER. „Postconditioning: Reperfusion of “reperfusion injury” after hibernation“. Cardiovascular Research 69, Nr. 1 (Januar 2006): 1–3. http://dx.doi.org/10.1016/j.cardiores.2005.11.011.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
33

Sakuma, Tsutomu, Keiji Takahashi, Nobuo Ohya, Osamu Kajikawa, Thomas R. Martin, Kurt H. Albertine und Michael A. Matthay. „Ischemia-reperfusion lung injury in rabbits: mechanisms of injury and protection“. American Journal of Physiology-Lung Cellular and Molecular Physiology 276, Nr. 1 (01.01.1999): L137—L145. http://dx.doi.org/10.1152/ajplung.1999.276.1.l137.

Der volle Inhalt der Quelle
Annotation:
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.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
34

Kang, K. J. „Mechanism of hepatic ischemia/reperfusion injury and protection against reperfusion injury“. Transplantation Proceedings 34, Nr. 7 (November 2002): 2659–61. http://dx.doi.org/10.1016/s0041-1345(02)03465-6.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
35

Rubin, B. B., S. Liauw, J. Tittley, A. D. Romaschin und P. M. Walker. „Prolonged adenine nucleotide resynthesis and reperfusion injury in postischemic skeletal muscle“. American Journal of Physiology-Heart and Circulatory Physiology 262, Nr. 5 (01.05.1992): H1538—H1547. http://dx.doi.org/10.1152/ajpheart.1992.262.5.h1538.

Der volle Inhalt der Quelle
Annotation:
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.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
36

Pemberton, M., G. Anderson, V. Vĕtvicka, D. E. Justus und G. D. Ross. „Microvascular effects of complement blockade with soluble recombinant CR1 on ischemia/reperfusion injury of skeletal muscle.“ Journal of Immunology 150, Nr. 11 (01.06.1993): 5104–13. http://dx.doi.org/10.4049/jimmunol.150.11.5104.

Der volle Inhalt der Quelle
Annotation:
Abstract Reperfusion of ischemic tissue is associated with tissue injury greater than that resulting from ischemia alone. C activation has been hypothesized to mediate the so-called ischemia/reperfusion injury through both membrane attack and C5a-dependent recruitment of neutrophils to sites of C3 fixation on the endothelium via C3 receptors. Adherence of neutrophils is preconditional to expression of their deleterious effects, which are central to the pathophysiology of ischemia/reperfusion injury. This study was designed to evaluate the effect of inhibition of C activation on ischemia/reperfusion injury using a soluble and truncated recombinant human CR1 (sCR1) molecule, a "tail-less" form of the membrane C3b/C4b receptor (CD35) that functions as a regulator of C activation. Capillary perfusion and leukocyte adherence to venular endothelium were measured after reperfusion in a mouse cremaster muscle model that allowed microscopic video observation of microcirculatory changes. Infusion i.v. with sCR1 before a 4-h period of ischemia and during a 3-h subsequent period of reperfusion prevented the increase in leukocyte adherence to venular endothelium seen in controls, and enhanced the number of reperfusing capillaries by 55%. Trypan blue staining showed an increase in muscle cell viability from 11 to 50% in mice receiving sCR1 as compared to controls. Tests of blood samples from mice infused with sCR1 demonstrated nearly complete inhibition of the mouse alternative pathway of C activation, but no detectable loss of the mouse classical pathway of C activation. It was concluded that C activation in this model of skeletal muscle injury is likely to be due to the alternative pathway, and that inhibition of C activation during reperfusion inhibits leukocyte adherence to blood vessel walls and protects the capillary microcirculation.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
37

Goldfarb, R. D., und A. Singh. „GSH and reperfusion injury.“ Circulation 80, Nr. 3 (September 1989): 712–13. http://dx.doi.org/10.1161/circ.80.3.2766517.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
38

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

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
39

Opie, Lionel H. „Mechanisms of reperfusion injury“. Current Opinion in Cardiology 6, Nr. 6 (Dezember 1991): 864–67. http://dx.doi.org/10.1097/00001573-199112000-00002.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
40

Ostadal, Petr. „What is ‘reperfusion injury’?“ European Heart Journal 26, Nr. 1 (30.11.2004): 99. http://dx.doi.org/10.1093/eurheartj/ehi029.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
41

Tosaki, Arpad, Anne Hellegouarch und Pierre Braquel. „Cicletanine and Reperfusion Injury“. Journal of Cardiovascular Pharmacology 17, Nr. 4 (April 1991): 551–59. http://dx.doi.org/10.1097/00005344-199104000-00005.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
42

Weight, S. C., P. R. F. Bell und M. L. Nicholson. „Renal ischaemia-reperfusion injury“. British Journal of Surgery 83, Nr. 2 (Februar 1996): 162–70. http://dx.doi.org/10.1046/j.1365-2168.1996.02182.x.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
43

Rushing, G. D., und L. D. Britt. „Reperfusion Injury After Hemorrhage“. Annals of Surgery 247, Nr. 6 (Juni 2008): 929–37. http://dx.doi.org/10.1097/sla.0b013e31816757f7.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
44

Clark, W. M. „Cytokines and reperfusion injury“. Neurology 49, Issue 5, Supplement 4 (01.11.1997): S10—S14. http://dx.doi.org/10.1212/wnl.49.5_suppl_4.s10.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
45

Obermaier, Robert, Oliver Drognitz, Stefan Benz, Ulrich T. Hopt und Przemyslaw Pisarski. „Pancreatic Ischemia/Reperfusion Injury“. Pancreas 37, Nr. 3 (Oktober 2008): 328–32. http://dx.doi.org/10.1097/mpa.0b013e31816d9283.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
46

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

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
47

Frank, Anja, Megan Bonney, Stephanie Bonney, Lindsay Weitzel, Michael Koeppen und Tobias Eckle. „Myocardial Ischemia Reperfusion Injury“. Seminars in Cardiothoracic and Vascular Anesthesia 16, Nr. 3 (23.02.2012): 123–32. http://dx.doi.org/10.1177/1089253211436350.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
48

Weyker, Paul D., Christopher A. J. Webb, David Kiamanesh und Brigid C. Flynn. „Lung Ischemia Reperfusion Injury“. Seminars in Cardiothoracic and Vascular Anesthesia 17, Nr. 1 (05.10.2012): 28–43. http://dx.doi.org/10.1177/1089253212458329.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
49

Bascom, John U., Peter Gosling und Bashir A. Zikria. „Hepatic ischemia-reperfusion injury“. American Journal of Surgery 184, Nr. 1 (Juli 2002): 84. http://dx.doi.org/10.1016/s0002-9610(01)00838-8.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
50

Soler-Soler, J. „Trimetazidine and reperfusion injury“. European Heart Journal 22, Nr. 11 (01.06.2001): 975. http://dx.doi.org/10.1053/euhj.2000.2529.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
Die Auswahlen zum Thema "Reperfusion injury" für andere Quellenarten können Sie auch interessieren:
Dissertationen Bücher
Wir bieten Rabatte auf alle Premium-Pläne für Autoren, deren Werke in thematische Literatursammlungen aufgenommen wurden. Kontaktieren Sie uns, um einen einzigartigen Promo-Code zu erhalten!

Zur Bibliographie