Revisiting Cerebral Postischemic Reperfusion Injury: New Insights in Understanding Reperfusion Failure, Hemorrhage, and Edema

2015 ◽  
Vol 10 (2) ◽  
pp. 143-152 ◽  
Author(s):  
Jilin Bai ◽  
Patrick D. Lyden
Keyword(s):  
Reperfusion Injury ◽  
Postischemic Reperfusion

Reduction of Postischemic Reperfusion Injury by the Vasoactive Drug Buflomedil

1991 ◽  
Vol 28 (1) ◽  
pp. 8-14
Author(s):  
Dirk Nolte ◽  
Hans-Anton Lehr ◽  
Falk-Udo Sack ◽  
Konrad Messmer
Keyword(s):  
Reperfusion Injury ◽  
Vasoactive Drug ◽  
Postischemic Reperfusion

Past and present course of cardioprotection against ischemia- reperfusion injury

2007 ◽  
Vol 103 (6) ◽  
pp. 2129-2136 ◽  
Author(s):  
David A. Liem ◽  
Henry M. Honda ◽  
Jun Zhang ◽  
David Woo ◽  
Peipei Ping
Keyword(s):  
Reperfusion Injury ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Permeability Transition ◽  
Reperfusion Therapy ◽  
Cardioprotective Effect ◽  
Western Society ◽  
Cardiovascular Research ◽  
Postischemic Reperfusion

Despite tremendous advances in cardiovascular research and clinical therapy, ischemic heart disease remains the leading cause of serious morbidity and mortality in western society and is growing in developing countries. For the past 5 decades, many scientists have studied the pathophysiology of myocardial ischemia-reperfusion (I/R) injury leading to infarction. With the exception of reperfusion therapy, attempts to salvage the myocardium during an acute myocardial infarction showed disappointing results in directly decreasing infarct size. Nevertheless, the phenomena of ischemic preconditioning and ischemic postconditioning show a consistent and robust cardioprotective effect in every used experimental animal model. As a result, many studies have focused on the intracellular protective signaling pathways that are involved in preconditioning and postconditioning. More recently, it has been suggested that components of the reperfusion injury salvage kinases pathway, protein kinase B, and the extracellular signal-regulated kinases can induce cardioprotection against I/R injury when they are activated during the postischemic reperfusion period. In addition, inhibition of mitochondrial permeability transition during postischemic reperfusion also shows a strong cardioprotective effect against I/R injury. The present mini-review highlights a short summary of the historical and present course of research into cardioprotection against myocardial I/R injury.

Biliary drainage attenuates postischemic reperfusion injury in the cholestatic rat liver

Surgery ◽  
2008 ◽  
Vol 144 (1) ◽  
pp. 22-31 ◽  
Author(s):  
J.J. Kloek ◽  
H.A. Marsman ◽  
A.K. van Vliet ◽  
D.J. Gouma ◽  
T.M. van Gulik
Keyword(s):  
Reperfusion Injury ◽  
Rat Liver ◽  
Biliary Drainage ◽  
Postischemic Reperfusion

scholarly journals Attenuation of postischemic reperfusion injury in striated skin muscle by diaspirin-cross-linked Hb

1998 ◽  
Vol 275 (2) ◽  
pp. H361-H368 ◽  
Author(s):  
Sven Pickelmann ◽  
Dirk Nolte ◽  
Rosmarie Leiderer ◽  
Elke Schütze ◽  
Konrad Messmer
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Oxygen Carrier ◽  
Isotonic Saline ◽  
Oxygen Carriers ◽  
Electron Microscopic ◽  
Platinum Surface ◽  
Early Reperfusion ◽  
Postischemic Reperfusion ◽  
Local Tissue

Hemoglobin-based oxygen carriers have been suggested to enhance the formation of oxygen free radicals, especially under conditions of ischemia-reperfusion (I/R), in which activation and adhesion of leukocytes play a pivotal role for propagation of reperfusion injury. This study investigates the effects of the hemoglobin-based oxygen carrier diaspirin-cross-linked hemoglobin (DCLHb) in an I/R model of hamster striated skin muscle. The dorsal skinfold chamber model in the awake Syrian golden hamster was used for analysis of the microcirculation and local tissue [Formula: see text]in striated skin muscle utilizing the technique of intravital fluorescence microscopy and a multiwire platinum surface (Clark type) electrode. Measurements were made before 4 h of pressure-induced ischemia and at 0.5, 2, and 24 h of reperfusion. Animals were treated with 5 ml/kg body wt of either 10% DCLHb ( n = 8), 6% Dextran 60 (Dx-60; 60 kDa, n = 8), or 0.9% NaCl ( n = 7), which was given intravenously 15 min before reperfusion. In animals treated with DCLHb or Dx-60, a significant decrease of leukocytes rolling along and sticking in postcapillary venules, associated with a recovery of functional capillary density and red blood cell velocity, was observed compared with saline-treated controls. In the early reperfusion period (0.5 h), DCLHb and Dx-60 efficiently restored local tissue[Formula: see text], whereas tissue[Formula: see text] decreased from 18.3 ± 1.9 to 15.3 ± 5.3 mmHg in 0.9% NaCl-treated animals. Electron microscopic analysis of the postischemic tissue at 24 h of reperfusion revealed markedly reduced tissue damage in animals treated with DCLHb compared with Dx-60 or isotonic saline. These results indicate that DCLHb attenuates postischemic reperfusion injury of striated skin muscle, presumably through alterations of leukocyte-endothelial cell interactions.

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