Key Points
- To determine whether calcium channel blockers exert direct protective effects against anoxia in isolated cardiac myocytes and to elucidate their mechanism of cardioprotection.
- Isolated calcium-tolerant rat cardiac myocytes were incubated under aerobic or anaerobic conditions in resting and electrically paced (300/min for 10 min) states, with or without 1 µM verapamil or 1 µM nifedipine.
- Cell injury was evaluated through rod-shaped cell morphology preservation, cellular ATP content, intracellular ion shifts (Na+, K+, and Ca2+), and lactate dehydrogenase release.
- Resting anoxic myocytes exhibited loss of rod morphology, significant ATP reduction, Na+ gain, K+ loss, and a twofold increase in lactate dehydrogenase release, with 1 µM verapamil or nifedipine providing no protection and leading to higher cellular Ca2+ upon reoxygenation.
- In anoxic myocytes paced at 300/min, 1 µM verapamil and 1 µM nifedipine significantly preserved rod morphology and cellular ATP levels compared to untreated paced anoxic controls, but the protected cells failed to sustain contractions at the pacing frequency.
Structured PICO
Do verapamil or nifedipine protect isolated rat cardiac myocytes from anoxic injury?
PPopulationIsolated Ca2+-tolerant rat cardiac myocytes
IInterventionVerapamil (1 microM) or nifedipine (1 microM) under aerobic or anaerobic conditions, in resting and contractile states
CComparatorControl aerobic or anaerobic cells without verapamil or nifedipine
OOutcomeProtection against cell injury assessed by preservation of rod-shaped morphology, cellular ATP levels, intracellular ionic composition, and lactate dehydrogenase releasesurrogate
Verapamil and nifedipine protect paced, but not resting, isolated rat cardiac myocytes from anoxic injury, suggesting the protective effect is related to reducing contractile demand rather than a direct cellular protective mechanism.