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Peri-infarct depolarization

We have seen that sodium enters the cells, but potassium is set free into the extracellular space where it induces irregular depolarizations, particularly in the surroundings of an ischemic focus. Such transient depolarizations travel over the cortex like classical waves of spreading depression of electrical activity (Back et al. 1994b Leao 1944 Nedergaard and Astrup 1986). The number of such peri-infarct depolarizations (PIDs) correlated well with final... [Pg.48]

Schuler OG, Eriskat J, Baethmann AJ, Back T (2001a) Thrombolysis induces a reperfusion-dependent inhibition of peri-infarct depolarizations in experimental thromboembolic stroke. J Cereb Blood Flow Metab 21 S396 Schuler OG, Plesnila N, Otto D, Baethmann AJ, Back T (2001b) Early thrombolysis inhibits periinfarct depolarizations in embolic MCA occlusion. NeuroReport 12 3943-3946 Schwindt W, Burke M, Pillekamp F, Luhmann HJ, Hoehn M (2004) Functional magnetic resonance imaging and somatosensory evoked potentials in rats with a neonatally induced freeze lesion of the somatosensory cortex. J Cereb Blood FlowMetab 24 1409-1418... [Pg.72]

Disturbances of proton diffusion are not unique to cerebral ischemia. Reduced diffusion has also been found in various experimental conditions including spreading depression (Busch et al. 1995) and peri-infarct depolarizations (Gyngell et al. 1994 Rother et al. 1996), hypoglycemia (Hasegawa et al. 1996), following cortical application of noxious substances [blockers of the Na+-/K+-ATPase (Benveniste et al. 1992), excitotoxins (Verheul et al. 1994)] and... [Pg.119]

Fig. 1.2 Putative cascade of damaging events in focal cerebral ischemia. Very early after the onset of the focal perfusion deficit, excitotoxic mechanisms can damage neurones and glia lethaUy. In addition, excitotoxicity triggers a number of events that can further contribute to the demise of the tissue. Such events include peri-infarct depolarizations and the more-delayed mechanisms of inflammation and programmed cell death. The x-axis reflects the evolution of the cascade over time, while the y-axis aims to illustrate the impact of each element of the cascade on final outcome (courtesy of Dimagl et al. 1999)... Fig. 1.2 Putative cascade of damaging events in focal cerebral ischemia. Very early after the onset of the focal perfusion deficit, excitotoxic mechanisms can damage neurones and glia lethaUy. In addition, excitotoxicity triggers a number of events that can further contribute to the demise of the tissue. Such events include peri-infarct depolarizations and the more-delayed mechanisms of inflammation and programmed cell death. The x-axis reflects the evolution of the cascade over time, while the y-axis aims to illustrate the impact of each element of the cascade on final outcome (courtesy of Dimagl et al. 1999)...
Strong AJ, Smith SE, Whittington DJ, Meldrum BS, Parsons AA, Krupinski J, Hunter AJ, Patel S, Robertson C. Eactors influencing the frequency of fluorescence transients as markers of peri-infarct depolarizations in focal cerebral ischemia. Stroke. 2000 31 214-222... [Pg.17]

Hartings JA, RoUi ML, Lu XC, TorteUa PC. Delayed secondary phase of peri-infarct depolarizations after focal cerebral ischemia Relation to infarct growth and neuroprotection. J Neurosci. 2003 23 11602-11610... [Pg.18]

Shin HK, Dunn AK, Jones PB, Boas DA, Lo EH, Moskowitz MA, Ayata C. Normobaric hyperoxia improves cerebral blood flow and oxygenation, and inhibits peri-infarct depolarizations in experimental focal ischaemia. Brain. 2007 130 1631-1642... [Pg.23]

Of the available MRI and CT measurements, abnormalities detected on diffusion-weighted MR imaging (DWI) are considered the most reliable estimate of the infarct core. Within this region, cell death occurs via a variety of mechanisms including excitotoxicity, oxida-tive/nitrosative stress, inflammation, apoptosis, and peri-infarct depolarization [55]. The loss of cellular energy metabolism causes a failure of membrane ionic... [Pg.251]


See other pages where Peri-infarct depolarization is mentioned: [Pg.67]    [Pg.6]    [Pg.6]    [Pg.603]    [Pg.67]    [Pg.6]    [Pg.6]    [Pg.603]   
See also in sourсe #XX -- [ Pg.48 , Pg.119 , Pg.229 ]




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