© 1995 American Heart Association, Inc.
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Inositol Phosphate Release and Metabolism During Myocardial Ischemia and Reperfusion in Rat Heart
From the Cellular Biochemistry Laboratory (K.E.A., E.A.W.) and the Alfred Baker Medical Unit (A.M.D.), Baker Medical Research Institute, Prahran, Australia.
Correspondence to Dr Elizabeth Woodcock, Baker Medical Research Institute, Commercial Rd, Prahran 3181, Australia.
Abstract A detailed study of the effects of global myocardial
ischemia and reperfusion on inositol phosphate release and metabolism
has been undertaken by using isolated perfused rat hearts. Ischemia for
longer than 5 minutes caused a cessation of inositol phosphate
production, with inositol phosphates initially present accumulating
as isomers of inositol monophosphate. This inhibition was independent
of norepinephrine. In contrast, 2-minute reperfusion following
20-minute ischemia produced a rapid and transient release of inositol
phosphates that was dependent on the release of norepinephrine and
mediated by 
1-adrenergic receptors. By a number of
criteria, this reperfusion response was different from the
norepinephrine response in normoxic tissue. First, total release of
inositol phosphates was greater (466±37 compared with 345±29 cpm/mg
protein, P<.05). Second, inositol 1,4,5-trisphosphate was
released with postischemic reperfusion (103±18 to 207±11 pmol/mg
protein), whereas release was not detected in normoxic myocardium. In
agreement with this, neomycin (0.5 and 5 mmol/L) inhibited inositol
phosphate release only under reperfusion conditions. Third, the
reperfusion response, unlike the response in nonischemic tissue,
required extracellular Ca2+. Longer periods of reperfusion
resulted in a return to a pattern of inositol phosphate release that
was not different from that seen in normoxic tissue. The rapid and
transient release of inositol 1,4,5-trisphosphate at 2-minute
postischemic reperfusion provides an explanation for the enhanced role
of 1-adrenergic receptors under these conditions and
suggests an important role for this compound in initiating
reperfusion-induced pathological events.
Key Words: inositol 1,4,5-trisphosphate • rat hearts • myocardial ischemia • reperfusion
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