Ke. Anderson et al., REPERFUSION FOLLOWING MYOCARDIAL-ISCHEMIA ENHANCES INOSITOL PHOSPHATERELEASE IN THE ISOLATED-PERFUSED RAT-HEART, Clinical and experimental pharmacology and physiology, 21(2), 1994, pp. 141-144
1. Global myocardial ischaemia (MI) for periods greater than 5 min cau
sed an inhibition of phosphatidylinositol specific phospholipase C (Pt
dIns-PLC) activity. 2. Two min reperfusion following a 20 min MI perio
d, a time point associated with reperfusion-induced arrhythmias, resul
ted in an activation of PtdIns-PLC activity, dependent on endogenous n
oradrenaline and mediated via alpha(1)-adrenoceptors. 3. This 2 min re
perfusion response, in contrast to healthy myocardium, resulted in: (i
) enhanced PtdIns-PLC activity; (ii) increased sensitivity to endogeno
us noradrenaline; (iii) rapid increases in inositol(l,4,5) trisphospha
te (Ins(1,4,5)P-3); and (iv) PLC hydrolysis primarily of PtdIns(4,5)Pz
, such that the majority of InsP isomers derive from Ins(1,4,5)P-3. 4.
Together, these data suggest a functional role for Ins(1,4,5)P-3 unde
r post-ischaemic reperfusion conditions, and provide a possible link b
etween alpha(1)-adrenoceptor stimulation of the PtdIns turnover pathwa
y and reperfusion injury.