The relationship between alterations in tissue
phospholipid composition and disruption of the plasma membrane during
ischemia in dog heart was examined using a homogeneous in vitro model of total
ischemia. This preparation was known to be associated with signs of membrane damage and was ideal for quantitation of
phospholipid changes in
ischemia because the weight of the tissue is unaffected by the duration of
ischemia and because there is no collateral flow to remove the endproducts of
phospholipid degradation. Measurements of
phospholipid phosphate per gram of tissue confirmed that recovery of
phospholipids and their degradation products was essentially complete in all samples including a sample taken after 24 h
ischemia. The results showed that
lysophospholipids gradually accumulated in the ischemic tissue; after 24 h in vitro
ischemia, they comprised 12% of the total tissue
phospholipids. Discontinuities of the plasma membrane were detected ultrastructurally in myocardium subjected to 150 min total
ischemia, while under the same conditions, the
lysophospholipid content amounted to less than 1% of the total tissue
phospholipids.
Phospholipid degradation was not limited by
calcium availability since the rate of lysolipid production was not enhanced by incubation of myocardial tissue in a medium containing 1.25 mM
calcium despite ultrastructural evidence of antecedent plasma membrane disruption. These data indicate that
lysophospholipids accumulate in ischemic myocardium in the absence of collateral flow or inflammatory cell infiltration but that
lysophospholipid accumulation occurs slowly and does not appear to be the dominant mechanism of plasma membrane fragmentation.