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Ischaemia cascade

Normally, the cascade from oxygen to water is well controlled by SOD, catalase and endogenous antioxidants such as glutathione, ascorbate and vitamin E. Vitamin E is the most important membrane-bound antioxidant. However, during ischaemia, the local control of ROS is lost, thus reactive free radicals can attack the membranes and lipid peroxidation begins. Endogenous antioxidants can be supplemented. This section describes this supplementation strategy. [Pg.267]

Pathophysiologically, thrombosis is the same sequence of events but now occurring in abnormal anatomical sites with intravascular obstruction that results in distal tissue ischaemia. These are often systemic disorders affecting the whole circulation and are described as hypercoagulable syndromes. Defects may lie at the level of the endothelium, inappropriate activation of the coagulation cascade or impaired activity of the fibrinolytic system. Segments of thrombus can become detached and travel peripherally in arterial tree, giving rise to acute insufficiency. Conversely, on the venous side, these are... [Pg.745]

There is no doubt that silent ischaemia, a term introduced by Stern and Tzivoni (1974), exists and represents lack of myocardial perfusion before the presence of pain or equivalents (Nesto and Kowal-druk, 1987) (ischaemic cascade - Figure 12.1). It is frequently seen in both patients with ACS and those with chronic IHD (Cohn, 1980, 2001 Cohn, Fox and Daly, 2003 Deanfield et at, 1984 Stern, 1998 Stern and Tzivoni, 1974). [Pg.302]

It is also clear, and has been established for some time now, that some neurons are susceptible to relatively short periods of ischaemia while others are not. Initially there are changes in the biochemical activity of neurons, in parallel with other cell types, which precede progressive tissue destruction. Although both types of neurons demonstrate similar morphological responses initially, susceptible neurons, perhaps due to differences in the biochemistry of some structural cytoskeletal components, for example, enter a postischaemic pathological cascade culminating in their death between 2 and 4 days and later after the ischaemic episode. However, despite a great deal of work which has attempted to unravel these complex intracellular processes, there is still not a clear and simple overview available. It is also apparent that for... [Pg.35]

Deby, C., Pincemail, J., Hans, P., Braquet, R, Lion, Y., Deby-Dupont, G., Goutier, R., 1984 Mechanisms of free radical production in the A A cascade and role of antilipoperoxidants and free radical scavengers, pp. 249-258. In Cerebral Ischaemia (Bes, A., Braquet, R, Paoletti, R., Siesjo, B. K., eds.). Elsevier Science Publishers BV. [Pg.70]


See other pages where Ischaemia cascade is mentioned: [Pg.76]    [Pg.80]    [Pg.87]    [Pg.89]    [Pg.263]    [Pg.264]    [Pg.270]    [Pg.165]    [Pg.701]    [Pg.701]    [Pg.372]    [Pg.431]    [Pg.431]    [Pg.19]    [Pg.172]    [Pg.242]    [Pg.215]    [Pg.492]    [Pg.55]   
See also in sourсe #XX -- [ Pg.302 ]




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Ischaemia

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