scholarly journals Hypoxic preconditioning protects rat hearts against ischaemia-reperfusion injury: role of erythropoietin on progenitor cell mobilization

2008 ◽  
Vol 586 (23) ◽  
pp. 5757-5769 ◽  
Author(s):  
Jih-Shyong Lin ◽  
Yih-Sharng Chen ◽  
Han-Sun Chiang ◽  
Ming-Chieh Ma
Keyword(s):  
Reperfusion Injury ◽  
Progenitor Cell ◽  
Hypoxic Preconditioning ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Rat Hearts ◽  
Cell Mobilization

scholarly journals Diabetes impairs progenitor cell mobilisation after hindlimb ischaemia–reperfusion injury in rats

Diabetologia ◽  
2006 ◽  
Vol 49 (12) ◽  
pp. 3075-3084 ◽  
Author(s):  
G. P. Fadini ◽  
S. Sartore ◽  
M. Schiavon ◽  
M. Albiero ◽  
I. Baesso ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Progenitor Cell ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

Role of complement regulatory membrane proteins in ischaemia-reperfusion injury of rat gastric mucosa

1999 ◽  
Vol 14 (10) ◽  
pp. 967-972 ◽  
Author(s):  
Fumihiro Iwata ◽  
Takashi Joh ◽  
Toyohiro Tada ◽  
Noriko Okada ◽  
B Paul Morgan ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Membrane Proteins ◽  
Reperfusion Injury ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Rat Gastric Mucosa

Hypoxic preconditioning in renal ischaemia–reperfusion injury: a review in pre-clinical models

2021 ◽  
Vol 135 (23) ◽  
pp. 2607-2618
Author(s):  
Laurie Bruzzese ◽  
Gwénaël Lumet ◽  
Donato Vairo ◽  
Claire Guiol ◽  
Régis Guieu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Potential Benefit ◽  
Graft Function ◽  
Major Complication ◽  
Hypoxic Preconditioning ◽  
Cellular Damage ◽  
Post Transplantation ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Clinical Models

Abstract Ischaemia–reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) and chronic kidney disease, which consists of cellular damage and renal dysfunction. AKI is a major complication that is of particular concern after cardiac surgery and to a lesser degree following organ transplantation in the immediate post-transplantation period, leading to delayed graft function. Because effective therapies are still unavailable, several recent studies have explored the potential benefit of hypoxic preconditioning (HPC) on IRI. HPC refers to the acquisition of increased organ tolerance to subsequent ischaemic or severe hypoxic injury, and experimental evidences suggest a potential benefit of HPC. There are three experimental forms of HPC, and, for better clarity, we named them as follows: physical HPC, HPC via treated-cell administration and stabilised hypoxia-inducible factor (HIF)-1α HPC, or mimicked HPC. The purpose of this review is to present the latest developments in the literature on HPC in the context of renal IRI in pre-clinical models. The data we compiled suggest that preconditional activation of hypoxia pathways protects against renal IRI, suggesting that HPC could be used in the treatment of renal IRI in transplantation.

The role of oxygen free radicals in the ischaemia - reperfusion injury

1987 ◽  
pp. 337-346
Author(s):  
F. Cuccurullo ◽  
A. Mezzetti ◽  
A. Arduini ◽  
E. Porreca ◽  
D. Lapenna ◽  
...  
Keyword(s):  
Free Radicals ◽  
Reperfusion Injury ◽  
Oxygen Free Radicals ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

scholarly journals Different mechanisms of mitochondrial proton leak in ischaemia/reperfusion injury and preconditioning: implications for pathology and cardioprotection

2006 ◽  
Vol 395 (3) ◽  
pp. 611-618 ◽  
Author(s):  
Sergiy M. Nadtochiy ◽  
Andrew J. Tompkins ◽  
Paul S. Brookes
Keyword(s):  
Reperfusion Injury ◽  
Kinase Inhibitor ◽  
Adenine Nucleotide ◽  
Treatment Strategies ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Rat Hearts ◽  
Perfused Rat Hearts

The mechanisms of mitochondrial proton (H+) leak under various pathophysiological conditions are poorly understood. In the present study it was hypothesized that different mechanisms underlie H+ leak in cardiac IR (ischaemia/reperfusion) injury and IPC (ischaemic preconditioning). Potential H+ leak mechanisms examined were UCPs (uncoupling proteins), allosteric activation of the ANT (adenine nucleotide translocase) by AMP, or the PT (permeability transition) pore. Mitochondria isolated from perfused rat hearts that were subjected to IPC exhibited a greater H+ leak than did controls (202±27%, P<0.005), and this increased leakage was completely abolished by the UCP inhibitor, GDP, or the ANT inhibitor, CAT (carboxyattractyloside). Mitochondria from hearts subjected to IR injury exhibited a much greater amount of H+ leak than did controls (411±28%, P<0.001). The increased leakage after IR was weakly inhibited by GDP, but was inhibited, >50%, by carboxyattractyloside. In addition, it was inhibited by cardioprotective treatment strategies including pre-IR perfusion with the PT pore inhibitors cyclosporin A or sanglifehrin A, the adenylate kinase inhibitor, AP5A (diadenosine pentaphosphate), or IPC. Together these data suggest that the small increase in H+ leak in IPC is mediated by UCPs, while the large increase in H+ leak in IR is mediated by the ANT. Furthermore, under all conditions studied, in situ myocardial O2 efficiency was correlated with isolated mitochondrial H+ leak (r2=0.71). In conclusion, these data suggest that the modulation of H+ leak may have important implications for the outcome of IR injury.

Sign in / Sign up

Export Citation Format

Share Document