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Subsequent Reperfusion (subsequent + reperfusion)

Distribution by Scientific Domains

Medical Sciences	83%

Selected Abstracts

Interleukin 18 causes hepatic ischemia/reperfusion injury by suppressing anti-inflammatory cytokine expression in mice

HEPATOLOGY, Issue 3 2004
Dan Takeuchi
Hepatic ischemia/reperfusion injury is a clinically important problem. While the mechanisms of the initial event and subsequent neutrophil-dependent injury are somewhat understood, little is known about the regulation of endogenous hepatoprotective effects on this injury. Interleukin 12 (IL-12) plays a role in the induction of this injury, but involvement of interleukin 18 (IL-18) has not been clarified. Using a murine model of partial hepatic ischemia and subsequent reperfusion, the aim of the current study was to determine whether IL-18 is up-regulated during hepatic ischemia/reperfusion and to determine the role of endogenous IL-18 in the development and regulation of inflammatory hepatic ischemia/reperfusion injury. Hepatic IL-18 expression was up-regulated from 1 to 8 hours after reperfusion. Hepatic ischemia/reperfusion induced nuclear factor-,B (NF-,B) and activator protein 1 (AP-1) activation, as defined by electrophoretic mobility shift assay, and caused significant increases in liver neutrophil recruitment, apoptosis, hepatocellular injury, and liver edema as defined by liver myeloperoxidase content, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick end-labeling (TUNEL) staining, serum aminotransferase levels, and liver wet-to-dry weight ratios. In mice treated with neutralizing antibody to IL-18, ischemia/reperfusion-induced increases in CXC chemokine expression, activation of NF-,B and AP-1, and apoptosis were greatly reduced. Furthermore, under blockade of IL-18, anti-inflammatory cytokines such as IL-4 and IL-10 were greatly up-regulated. Signal transducer and activator of transcription 6 (STAT6) was significantly activated under blockade of IL-18. These conditions also caused significant reduction in liver neutrophil sequestration and liver injury. In conclusion, the data suggest that IL-18 is required for facilitating neutrophil-dependent hepatic ischemia/reperfusion injury through suppressing anti-inflammatory cytokine expression. (HEPATOLOGY 2004;39:699,710.) [source]

EPR oximetry in the beating heart: Myocardial oxygen consumption rate as an index of postischemic recovery

MAGNETIC RESONANCE IN MEDICINE, Issue 4 2004
Govindasamy Ilangovan
Abstract Oxygen plays a critical role in the pathophysiology of myocardial injury during both ischemia and subsequent reperfusion (I/R). Thus, oxygen concentration is an important variable to measure during I/R. In the present work, electron paramagnetic resonance (EPR)-based oximetry was used to measure the oxygen concentration during a series of I/R episodes and oxygenation levels were correlated with the contractile and hemodynamic functions of the heart. A custom-developed electronically tunable surface coil resonator working at 1.1 GHz was used to determine tissue pO2 in the beating heart. Microcrystalline particulate of lithium phthalocyanine was used as an EPR oximetry probe. Isolated and perfused rat hearts were subjected to 1 or 3 hr durations of preischemic perfusion, followed by 15-min I/R cycles. In hearts perfused for 3 hr prior to 15-min I/R cycles, the myocardial pO2 decreased gradually on subsequent reperfusions of three successive I/R cycles. However, in hearts perfused for 1 hr there was almost 100% recovery of myocardial pO2 in all three I/R cycles. The extent of oxygenation recovered in each reperfusion cycle correlated with the recovery of hemodynamic and contractile function. The results also showed that the oxygen consumption rate of the heart at the end of each I/R episode decreased in direct proportion to the functional recovery. In summary, it was observed that the amount of myocardial oxygen consumption during I/R could provide a reliable index of functional impairment in the heart. Magn Reson Med 51:835,842, 2004. © 2004 Wiley-Liss, Inc. [source]

Effect of HTK on the microcirculation in the rat cremaster muscle during warm ischemia and reperfusion

MICROSURGERY, Issue 2 2005
Jacqueline Bastiaanse M.D.
Histidine-tryptophan-ketoglutarate (HTK) preserves rat muscle function during cold storage. We examined the effect of HTK perfusion on preservation of microvascular function during 4 h of warm ischemia and subsequent reperfusion (I/R) in the rat cremaster muscle. Leukocyte-endothelium interactions, capillary perfusion, and arteriole diameters were quantified prior to HTK-perfusion and/or ischemia, and at 0, 1, and 2 h after restoration of blood flow. In all groups, the number of rolling leukocytes increased with time, whereas I/R induced a slight increase in leukocyte adhesion. After ischemia, capillary perfusion rapidly recovered to about 50% and returned to near normal (90%) after 2 h. HTK at 22°C did not affect the assessed microcirculation variables, whereas HTK at 4°C reduced leukocyte rolling, but not adhesion. Therefore, microvascular function of HTK-perfused muscles was not better preserved during warm I/R than that of nonperfused muscles. Contrary to other preservation solutions, HTK perfusion in itself was not detrimental to the microcirculation. © 2005 Wiley-Liss, Inc. Microsurgery 25:174,180, 2005. [source]

Pharmacological delayed preconditioning against ischaemia-induced ventricular arrhythmias: effect of an adenosine A1 -receptor agonist

BRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2001
Renaud Tissier
The goal of this study was to investigate the effects of the delayed pharmacological preconditioning produced by an adenosine A1 -receptor agonist (A1 -DPC) against ventricular arrhythmias induced by ischaemia and reperfusion, compared to those of ischaemia-induced delayed preconditioning (I-DPC). Eighty-nine instrumented conscious rabbits underwent a 2 consecutive days protocol. On day 1, rabbits were randomly divided into four groups: ,Control' (saline, i.v.), ,I-DPC' (six 4-min coronary artery occlusion/4-min reperfusion cycles), ,A1 -DPC100' (N6 -cyclopentyladenosine, 100 ,g kg,1, i.v.), and ,A1 -DPC400' (N6 -cyclopentyladenosine, 400 ,g kg,1, i.v.). On day 2, i.e., 24 h later, the incidence and severity of ventricular arrhythmias during a 30-min coronary artery occlusion and subsequent reperfusion were analysed in all animals, using an arrhythmia score. I-DPC, A1 -DPC100 and A1 -DPC400 significantly reduced the infarct size (34±5, 42±3 and 43±7% of the area at risk, respectively) as compared to Control (55±3% of the area at risk). During both ischaemia and reperfusion, neither the incidence nor the severity of ventricular arrhythmias were altered by A1 -DPC100, A1 -DPC400 or I-DPC as compared to Control. Thus, despite reduction of infarct size induced by delayed preconditioning, A1 -DPC as well as I-DPC failed to exert any anti-arrhythmic effect in the conscious rabbit model of ischaemia-reperfusion. British Journal of Pharmacology (2001) 134, 1532,1538; doi:10.1038/sj.bjp.0704407 [source]

Effects of caffeic acid phenethyl ester and alpha-tocopherol on reperfusion injury in rat brain

CELL BIOCHEMISTRY AND FUNCTION, Issue 3 2003
M. Kemal Irmak
Abstract Oxygen-derived free radicals have been implicated in the pathogenesis of cerebral injury after ischaemia,reperfusion. Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, exhibits antioxidant properties. The purpose of the present study was to investigate the effects of ischaemia and subsequent reperfusion on rat brain and to investigate the effects of two free radical scavengers, CAPE and alpha-tocopherol, on this in vivo model of cerebral injury. Ischaemia was induced by bilateral occlusion of the carotid arteries for 20,min and reperfusion was achieved by releasing the occlusion to restore the circulation for 20,min. Control rats underwent a sham operation. CAPE at 10,,;mol,kg,1 or alpha-tocopherol at 25,,mol,kg,1 was administered intraperitoneally before reperfusion. Reperfusion led to significant increase in the activity of xanthine oxidase and higher malondialdehyde levels in the brain. Acute administration of both CAPE and alpha-tocopherol suppressed ischaemia,reperfusion-induced cerebral lipid peroxidation and injury, but CAPE seems to offer a better therapeutic advantage over alpha-tocopherol. Copyright © 2003 John Wiley & Sons, Ltd. [source]