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Ischaemia preconditioning

Stenzel-Poore MP, Stevens SL, Xiong Z, Lessov NS, Harrington GA, et al. 2003. Effect of ischaemic preconditioning on genomic response to cerebral ischaemia similarity to neuroprotective strategies in hibernation and hypoxia-tolerant states. Lancet 362 1028. [Pg.407]

Marais, E., Genade, S., Huisamen, B., Strijdom, J.G., Moolman, J.A., and Lochner, A. 2001b. Activation of p38 MAPK induced by a multi-cycle ischaemic preconditioning protocol is associated with attenuated p38 MAPK activity during sustained ischaemia and reperfusion. J. Mol. Cell. Cardiol. 33 769-778. [Pg.85]

Das, D. K. Engelman, R. M. Kimura, Y. Molecular adaptation of cellular defences following preconditioning of the heart by repeated ischaemia. Cardiovasc. Res. 27 578-584 1993. [Pg.57]

The effects of ischaemic preconditioning on hexose transport has been investigated in the Langendorff-perfused heart. Four cycles of 5 min of ischaemia followed by 5 min of reperfusion was used to precondition the hearts prior to measurement of 2DG uptake detected by P NMR measurements of the accumulation of 2-deoxy-glucose-6-phosphate (2DG6P). In preconditioned hearts, the accumulation of 2DG6P was greater than that in... [Pg.405]

Protein kinase signal transduction pathways have been extensively studied and characterised in the myocardium. Much work has focussed on studying the role of individual kinases involved in ischaemic preconditioning (IP). IP describes the reduction in susceptibility to myocardial infarction that follows brief periods of sublethal ischaemia (Muny et al., 1986). This reduction can manifest itself as a 4-fold reduction in infarct size, this being secondary to a delay in the onset and rate of cell necrosis during the subsequent lethal ischaemia (Marber et al., 1994). [Pg.38]

Preconditioning motor activity for 15 min significantly enhanced the resistance of CAl pyramidal neurones to ischaemia at a temperature of 30 °C (Gerasimov et al. 2001). The period of protection lasted for up to 40 min after the end of motor activity, When ischaemia was started within 5-10 min after the preconditioning, complete restoration of the field potentials to preischaemic control levels could be achieved. [Pg.500]

Both ischaemia (clamping of the superior mesenteric artery for 30,60, 90 min) and ischaemia/reperfusion affected respiratory function of isolated rat enterocyte mitochondria as compared to control (Madesh et al. 2000). Preconditioning with nitric oxide donor, sodium nitroprusside (1 mM, given into the proximal jejunal lumen at a rate of 1 ml/ min), significantly enhanced the recovery of the respiratory control rate. Mitochondrial lipid changes suggestive of activation of phospholipase... [Pg.623]

The role of reactive oxygen species and mitochondrial KATPase channels in the cardioprotective effects of ischaemic preconditioning or treatment with diazoxide have been investigated in the isolated rat heart. Treatment with diazoxide improved coronary flow rate and LVDP after ischaemia-reperfusion compared to control hearts, and this affect was abolished by treatment with the KATPase channel opener 5-hydroxydecanoate or the antioxidant V-acetylcy-steine. Ischaemic preconditioning also improved coronary flow rate and LVDP after ischaemia-reperfusion, however, this was not affected by treatment with 5-hydroxydecanoate or V-acetylcysteine. Treatment with diazoxide or... [Pg.467]


See other pages where Ischaemia preconditioning is mentioned: [Pg.71]    [Pg.71]    [Pg.61]    [Pg.196]    [Pg.197]    [Pg.197]    [Pg.199]    [Pg.406]    [Pg.617]    [Pg.476]    [Pg.477]    [Pg.481]    [Pg.490]    [Pg.580]    [Pg.589]    [Pg.468]    [Pg.31]    [Pg.533]   
See also in sourсe #XX -- [ Pg.580 ]




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