Myocardial ischemia-reperfusion injury is a medical problem occurring as damage to the myocardium following blood flow restoration after a critical period of coronary occlusion. Oxygen free radicals (OFR) are implicated in reperfusion injury after myocardial ischemia. The antioxidant enzyme, Cu, Zn-superoxide dismutase (Cu, Zn-SOD, also called SOD1) is one of the major means by which cells coun...

BACKGROUND AND PURPOSE We recently demonstrated that endogenous nitric oxide (NO) modulates collateral blood flow in a neonatal stroke model in rats. The inhalation of NO (iNO) has been found to be neuroprotective after ischemic brain damage in adults. Our objective was to examine whether iNO could modify cerebral blood flow during ischemia-reperfusion and reduce lesions in the developing brain...

A specific action against myocardial reperfusion injury of the oxygen paradox type was recently characterized for halothane after anoxic perfusion in isolated rat hearts and isolated cardiomyocytes. In this study, we have characterized the protective effects of the clinically available inhalation anaesthetics during reperfusion after ischaemia. In isolated, isovolumically beating rat hearts per...

Aldehyde dehydrogenase 2 (ALDH2) is an important factor in inhibiting oxidative stress and has been shown to protect against renal ischemia/reperfusion injury. Therefore, we hypothesized that ALDH2 could reduce spinal cord ischemia/reperfusion injury. Spinal cord ischemia/reperfusion injury was induced in rats using the modified Zivin's method of clamping the abdominal aorta. After successful m...

We investigated the role of the Wnt signaling pathway in cerebral ischemia/reperfusion injury by examining β-catenin and glycogen synthase kinase-3β protein expression in the rat hippocampal CA1 region following acute cerebral ischemia/reperfusion. Our results demonstrate that cell apoptosis increases in the CA1 region following ischemia/reperfusion. In addition, β-catenin and glycogen synthase...

The effect of the antioxidant drug “U-74389G” was examined, on rat model and particularly in an oviductal ischemia reperfusion (IR) protocol. The probable effects of that molecule were studied pathologically using oviductal congestion (OC) lesions. 40 rats of mean weight 231.875 g were used in the study. OC lesions were evaluated at 60 min of reperfusion (groups A and C) and at 120 min of reper...

BACKGROUND Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in cardiac contractile dysfunction as well as cardiomyocyte injury. These deleterious effects are due in large part to endothelial dysfunction leading to the upregulation of cell adhesion molecules and subsequent neutrophil-endothelium interaction. At clinically relevant doses, simvastatin...

Indolamine 2,3-dioxygenase (IDO), an enzyme that catalyses the metabolism of tryptophan, may play a detrimental role in ischemia-reperfusion injury (IRI). IDO can be inhibited by 1-methyl-tryptophan, which exists D (D-MT) or L (L-MT) isomer. These forms show different pharmacological effects besides inhibition. Therefore, we sought to investigate whether these isomers protective renal IRI, eith...

introduction: development of brain edema following focal cerebral ischemia exacerbates primary ischemic injury. blood brain barrier (bbb) opening is an important part of edema named as vasogenic brain edema. in this study, quantitative alterations of bbb permeability is experimentally evaluated using transient focal cerebral ischemia in the rat. methods: two groups of male rats (ischemic and sh...

results in all groups ischemic changes were apparently observed in hippocampus ca1 neurons. in two-vessel occlusion model, after 3 and 24 hours of reperfusions, ischemic cells accounted for 14.9% and 23.2%, respectively. in four-vessel occlusion model, after 3 and 24 hours of reperfusions, ischemic cells accounted for 7.6% and 44.9% (p < 0.0001), respectively. background an appropriate animal m...