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  • Title: Reperfusion following myocardial ischaemia enhances inositol phosphate release in the isolated perfused rat heart.
    Author: Anderson KE, Dart AM, Woodcock EA.
    Journal: Clin Exp Pharmacol Physiol; 1994 Feb; 21(2):141-4. PubMed ID: 8039268.
    Abstract:
    1. Global myocardial ischaemia (MI) for periods greater than 5 min caused an inhibition of phosphatidylinositol specific phospholipase C (PtdIns-PLC) activity. 2. Two min reperfusion following a 20 min MI period, a time point associated with reperfusion-induced arrhythmias, resulted in an activation of PtdIns-PLC activity, dependent on endogenous noradrenaline and mediated via alpha 1-adrenoceptors. 3. This 2 min reperfusion response, in contrast to healthy myocardium, resulted in: (i) enhanced PtdIns-PLC activity; (ii) increased sensitivity to endogenous noradrenaline; (iii) rapid increases in inositol(1,4,5)trisphosphate (Ins(1,4,5)P3); and (iv) PLC hydrolysis primarily of PtdIns(4,5)P2, such that the majority of InsP isomers derive from Ins(1,4,5)P3. 4. Together, these data suggest a functional role for Ins(1,4,5)P3 under post-ischaemic reperfusion conditions, and provide a possible link between alpha 1-adrenoceptor stimulation of the PtdIns turnover pathway and reperfusion injury.
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