Reactive oxygen species (ROS) contribute to the ischemia-reperfusion injury. In kidney, the intracellular sources of ROS during ischemia-reperfusion are still unclear. In the present study, we investigated the role of the catecholamine-degrading enzyme monoamine oxidases (MAOs) in hydrogen peroxide (H2O2) generation after reperfusion and their involvement in cell events leading to tissue injury...

Endothelin (ET) receptor antagonism protects from ischemia-reperfusion injury. We hypothesized that the cardioprotective effect is related to nitric oxide (NO) bioavailability. Buffer-perfused rat and mouse hearts were subjected to ischemia and reperfusion. At the onset of ischemia, the rat hearts received vehicle, the dual endothelin type A/type B (ETA/ETB) receptor antagonist bosentan (10 mic...

Very early reperfusion after coronary occlusion can reduce infarct size and preserve left ventricular function. Whether later reperfusion is of benefit is unclear. We studied the effect of very early reperfusion with myocardial salvage and "late" reperfusion without myocardial salvage on infarct expansion and aneurysm formation. Sixty-eight rats underwent left coronary artery ligation and were ...

OBJECTIVES Loss of glutamate from cardiomyocytes during ischaemia may aggravate ischaemia-reperfusion injury in open heart surgery. This may be due to reversal of excitatory amino acid transporters (EAATs). However, the expression of such transporters in cardiomyocytes is ambiguous and quantitative data are lacking. Our objective was to study whether EAATs were expressed in the rat heart and to...

Selective troponin I (TnI) modification has been demonstrated to be in part responsible for the contractile dysfunction observed with myocardial ischemia/reperfusion injury. We have isolated and characterized modified TnI products in isolated rat hearts after 0, 15, or 60 minutes of ischemia followed by 45 minutes of reperfusion using affinity chromatography with cardiac troponin C (TnC) and an...

We have demonstrated that in vitro brief ischemia activates nuclear factor (NF)-kappaB in rat myocardium. We report in vivo ischemia-reperfusion (I/R)-induced NF-kappaB activation, IkappaB kinase -beta (IKKbeta) activity, and IkappaBalpha phosphorylation and degradation in rat myocardium. Rat hearts were subjected to occlusion of the coronary artery for up to 45 min or occlusion for 15 min foll...

Necroptosis has an important role in ischemia-reperfusion damage. The expression of histone deacetylase 6 (HDAC6) is upregulated in neurons following ischemia-reperfusion, however, whether HDAC6 is closely involved in the necroptosis, which occurs during ischemia-reperfusion damage remains to be elucidated. In the present study, the roles of HDAC6 in the necroptosis of cultured rat cortical neu...

Khimenko, Pavel L., G. J. Bagby, J. Fuseler, and Aubrey E. Taylor. Tumor necrosis factor-a in ischemia and reperfusion injury in rat lungs. J. Appl. Physiol. 85(6): 2005–2011, 1998.—The effects of both recombinant rat tumor necrosis factor-a (TNF-a) and an anti-TNF-a antibody were studied in isolated buffer-perfused rat lungs subjected to either 45 min of nonventilated [ischemia-reperfusion (I/...

OBJECTIVES Coronary venous retroinfusion (CVR) has been used experimentally in large animals for selective drug delivery into ischaemic myocardium. It would be an advantage if CVR could also be used in isolated perfused rat heart models. The aim of the present paper is to develop a regional ischaemic model in the isolated perfused rat heart combined with CVR. METHOD Pharmacokinetic study: The...

We attempted in the present study to clarify the preventive effects of cyclohexenonic long-chain fatty alcohol on ischemia-reperfusion injury in the rat bladder. Rat bladders were exposed to 30 min of ischemia and a subsequent 30 min of reperfusion with or without several doses of cyclohexenonic long-chain fatty alcohol (0.5, 2, 8 mg/kg). Muscle-bath studies were performed, and malonaldehyde co...