Ischaemia, ischaemic injury

Osborne, D.L., Carter, P.R., Aw, T.Y. and Kvietys, P.R. (1992). Attenuation of ischaemia/reperfusion injury by a previous ischaemic insult. Gastroenterology 102, A231. 

Inflammatory cell phenomenon are also contributors to lipid peroxidation. Activated neutrophils may adhere to damaged endothelium and amplify traumatic, ischaemic or ischaemia-reperfiision injury. Many cyclooxygenase products of the metabolism of atachidonic acid modulate the inflammatory responses of cells. Macrophages, neutrophils and microglia are important sources of reactive oxygen at the injury site. When activated, they produce a respiratory burst that is traced to activated nicotinamide adenine dinucleotide (NADPH/NADH) oxidase. 

Therefore, in clinical practice, the same correlation Q waves of necrosis in ECG leads and necrotic areas is used to locate injured areas (ST changes) or ischaemic ones (T-wave changes), although, very often in the acute phase, the ECG patterns of ischaemia and injury are usually visible in more leads than the ECG pattern of necrosis. However, in the chronic phase, the ECG pattern of injury usually... 

In conclusion, this section has highlighted the potential pathogenic contribution of blood neutrophils to the CNS injury that accompanies the ischaemia-reperfusion injury of stroke. From experimental models of this disorder, it appears that the second wave of tissue damage is induced either by neutrophil-mediated vasoocclusion or by the infiltration of neutrophils into the ischaemic tissue with concomitant release of lytic factors. Antagonising both neutrophil attachment to endothelium and the transendothelial migration of these cells at the level of the blood-brain barrier is likely to be of clinical benefit to cerebral ischaemia-reperfusion injury. Consequently, it is anticipated that a further unravelling of the mechanisms that promote neutrophil interaction with cerebral vessel walls will lead to the introduction of a more specific therapeutic intervention for the treatment of stroke. 

Lorente de No R (1934) Studies on the structure of the cerebral cortex. II. Continuation of the study of the Ammonic system. J Psychol Neurol 46 113-177 Love S, Barber R, Wilcock GK (1998) Apoptosis and expression of DNA repair proteins in ischaemic brain injury in man. Neuroreport 9 955-959 Love S, Barber R, Wilcock GK (1999) Neuronal accumulation of poly(ADP-ribose) after brain ischaemia. Neuropathol Appl Neurobiol 25 98-103 Luskin MB (1993) Restricted proliferation and migration of postnatally generated neurons derived from the forebrain subventricular zone. Neuron 11 173-189 Magavi SS, Leavitt BR, Macklis JD (2000) Induction of neurogenesis in the neocortex of adult mice. Nature 405 951-955... 

The electrocardiographic pattern of injury is recorded from the myocardial area in which, as a consequence of diminished blood supply (more important than the one that generates the ECG pattern of ischaemia) or other non-ischaemic causes, an evident diastolic cellular depolarisation exists (Figure 2.1(3)). This leads to the formation of a low-quality TAP in the injury area which is expressed in the ECG as ST-segment depression or elevation (see Experimental point of view - below - and Figure 4.5). This ECG pattern usually represents especially in the setting of ACS and especially, when the changes are dynamic, the existence of active ischaemia. 

Cinnamophilin has protective activity against reperfusion injury of the ischaemic skeletal muscle in rats. Ischaemia was induced in one hind limb by application of a tourniquet on the proximal thigh the contralateral limb served as an internal control. Of the four-reperfusion groups, only the cinnamophilin group had a smaller triphenyltetrazolium chloride reduction and lower muscle weight gain [302],... 

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