Key Points
- To identify the subcellular sites of phospholipid catabolism that govern the transition from reversible to irreversible ischemic injury in cardiac myocytes.
- Incubated neonatal rat cardiac myocytes with 5 nM [3H]arachidonic acid to trace loci of phospholipid turnover.
- Induced simulated reversible and irreversible ischemic injury using 30 μM iodoacetate and mapped subcellular alterations using quantitative electron microscopic autoradiography.
- Arachidonic acid incorporation into sarcolemmal phospholipids increased by 20-fold during reversible injury and 96-fold during irreversible injury relative to control conditions.
- Sarcolemmal phospholipid specific radioactivity increased by 5-fold in reversibly injured myocytes and 28-fold in irreversibly injured myocytes, with no significant alterations detected in other subcellular organelles.
Structured PICO
PPopulationNeonatal rat cardiac myocytes
IInterventionIncubation with 5 nM [3H]arachidonic acid and exposure to 30 microM iodoacetate to produce reversible and irreversible injury
CComparatorControl conditions
OOutcomePhospholipid catabolism and turnover in individual subcellular organelles (specifically sarcolemma)surrogate
Selective catabolism of sarcolemmal phospholipids appears to be a pivotal determinant of lethal myocardial injury during ischemia.