Arachidonic acid ischaemia

In platelets or other cells, stimulated by thrombin, bradykinin, ischaemia or by other means, there is an increased release of arachidonic acid, presumably to a large extent derived from hydrolysis of phospholipids (e.g. phosphatidylethanolamine, phosphatidylcholine and phosphatidylinositol). Phosphatidylethanolamine and phosphatidylcholine are generally believed to be hydrolysed by phospholipase Aj [26], while phosphatidylinositol is hydrolysed by phospholipase C and then by other lipases as discussed below. It is not known whether activation of these lipases are primary or secondary events in cell activation [23]. The activity of phospholipase A 2... 

A number of procedures are known to cause release of prostaglandins in the brain. Electrical stimulation, trauma, hypoxia, ischaemia, hypoglycemia, convulsion, pyrogen fever aU cause a rapid increase in free arachidonic acid and stimulation of prostaglandin biosynthesis. For general reviews of eicosanoids in the nervous system, see refs. 201 203. 

Isolated raf hearts subjected to 15 min ischaemia followed by 30 min reperfusion showed concomitant accumulation of free calcium (Indo-1 fluorescence technique) and degradation of membrane phosphoUpids as indicated by an increase of tissue arachidonic acid content (Ivanics et al. 2001). This observation is suggestive for a relationship the Ca -related fluorescence and arachidonic acid accumulation probably due to a calcium-mediated stimulation of phospholipase Aj. 

The determination of the amounts of arachidonate derivatives present in different compartments of the brain in vivo is extraordinarily difficult (Pickard and Walker 1984 a). Ischaemia leads to a rapid accumulation of free fatty acids, including arachidonic acid, in neural tissue (Bazan 1971). Bosisio et a/. (1976) showed that with cerebral ischaemia, there is a release of free arachidonic acid which is rapidly converted to prostaglandins. 

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