Ion Movements Early in Myocardial Ischaemia: Relation to Arrhythmias, Early Contractile Failure and Tissue Necrosis

Poole‐Wilson, Philip A.

doi:10.1007/978-1-349-12522-7_6

Cited by 1 publication

(1 citation statement)

References 47 publications

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“…However, other studies have shown palmitoyl carnitine to activate L-type calcium channels, leading to an increase in ICa(L) (13)(14)(15). An increase in the calcium current could also lead to shortening in the duration of the AP and PER by causing early inactivation of the L-type calcium channel and activation of outward potassium currents (26). An increase in Ica(L) would result in an initial positive inotropic effect and could eventually lead to a rise in resting diastolic tension if intracellular calcium levels increased.…”

Section: Electrophysiological Effects Of Palmitoyl Carnitinementioning

confidence: 96%

Effects of Palmitoyl Carnitine on Perfused Heart and Papillary Muscle

Patel

Economides

Byrne

1999

J Cardiovasc Pharmacol Ther

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BACKGROUND: Palmitoyl carnitine accumulation during ischemia causes profound electrophysiological changes, resulting in arrhythmias. We studied the electrophysiological and contractile effects of palmitoyl carnitine. METHODS AND RESULTS: Extracellular recordings made by using the endocardial unipolar paced evoked response (PER) in isolated perfused rabbit hearts were compared with action potentials (AP) recorded from septal artery perfused rabbit papillary muscle. Left ventricular pressure was monitored in isolated hearts. In perfused hearts palmitoyl carnitine (30 µmol/L, 30 minutes) significantly (P <.001) increased the latency of activation (St-R interval) by 58% +/- 8% and reduced repolarization time (R-E interval) by 39% +/- 4%. PER duration (St-E interval), was reduced by 30% +/- 3%. Palmitoyl carnitine (30 µmol/L) significantly (P <.001) decreased resting membrane potential (19 +/- 2 mV) of AP, reduced peak amplitude (33.5 +/- 8 mV) and rate of rise of phase 0 (41 +/- 8 V/s). Significant reductions (P <.001) in the action potential duration 50% (129.4 +/- 28 ms) and 90% (139.8 +/- 32 ms) were also observed. An initial positive inotropic effect, which declined as irreversible contracture developed, was also observed. Verapamil (1 µmol/L), nifedipine (1 µmol/L), and caffeine (10 mmol/L) failed to abolish the positive inotropy. CONCLUSIONS: We suggest that palmitoyl carnitine disrupts intracellular calcium homeostasis leading to disturbances in electrical and contractile activity. Its accumulation during myocardial ischemia could contribute to calcium overloading and initiate lethal arrhythmias.

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