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Normokalemic adenosine-lidocaine cardioplegia: importance of maintaining a polarized myocardium for optimal arrest and reanimation

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IN PRESS

by:
Kathryn L. Sloots, BSc (Hons) and Geoffrey P. Dobson Ph.D
Heart Research laboratory,
Dept Physiology and Pharmacology,
Molecular Science Building,
James Cook University, Townsville,
Queensland, Australia, 4811

Key Words:

warm cardioplegia, membrane potential, high potassium, depolarising, polarising, normothermia, organ preservation, heart, adenosine, lidocaine, adenocaine, myocardium, ischemia, cardiac surgery, reperfusion, cardioprotection

Abstract:
Objective: Depolarising potassium (K+) cardioplegia does not afford optimal cardioprotection in pediatric or adult patients requiring complicated operative procedures. Polarising adenosine-lidocaine (AL) cardioplegia has been shown to be cardioprotective without hyperkalemia. Our aim was to examine the effects of changing extracellular potassium in adenosine-lidocaine (AL) cardioplegia on arrest and reanimation properties.

Methods: Isolated-perfused rat hearts (n = 96) were arrested at 32-33°C for 1 or 2 hours with intermittent 200 uM adenosine and 500 uM lidocaine in modified Krebs-Henseleit (K-H) buffer with 0.1, 3.0, 5.9, 10 and 16 mM potassium (K+), or with 16 mM or 25 mM potassium (K+) in Krebs-Henseleit (K-H) (n=8 each group). Membrane potentials were estimated in the arrested ventricular myocardium (n = 42), and recovery function was measured in working mode during 60 min reperfusion.

Results: Arrest was interrupted by ‘breakout’ beats in adenosine-lidocaine (AL) hypokalemic (0.1 and 3 mM K+) and non-AL hyperkalemic (16 and 25 mM K+) hearts. The membrane potentials for non-AL 16 and 25 mM potassium (K+) hearts were -51 and -39 mV, and for adenosine-lidocaine (AL) hearts (0.1, 3.0, 5.9, 10 and 16 mM K+) were -183, -94, -75, -65 and -49 mV respectively. After 1 hour arrest, coronary vascular resistance (CVR) increased linearly in adenosine-lidocaine (AL) cardioplegia with increasing potassium (K+) (5.9, 10, 16 mM), and the slope increased over twofold after 2 hours. Nearly 40% ofadenosine-lidocaine (AL) (0.1 mM K+) and non-AL 25 mM K+ hearts failed to recover after 1 hour arrest. After 2 hours, polarising (5.9 mM K+) adenosine-lidocaine (AL) hearts increased CVR by only 30% and spontaneously recovered 107% heart rate, 92% systolic pressure, 81% aortic flow and 113% coronary flow (all metrics returned 85 to 100% at 15 min) with no reperfusion arrhythmias. In contrast, the adenosine-lidocaine (AL) (3, 10 and 16 mM K+) groups were all ‘slow-to-recover’ (15 to 40% return at 15 min) and experienced arrhythmias. Increasing potassium (K+) in adenosine-lidocaine (AL) cardioplegia from 5.9 to 16 mM resulted in a 67% loss of left ventricular contractility.

Conclusions: Polarising adenosine-lidocaine (AL) cardioplegia (5.9 mM K+) administered intermittently at 33°C provides superior arrest and reanimation profiles under normokalemic conditions when the myocardial cell membrane potential is close to its resting state.

Mini-abstract:
Adenosine-lidocaine (AL) cardioplegia was examined in the presence of 0.1, 3, 5.9, 10 and 16 mM potassium (K+) during 1 and 2 hours arrest at 33°C.  Adenosine-lidocaine (AL) cardioplegia demonstrated superior arrest and recovery profiles when the membrane potential was maintained around the resting cell voltage using physiological levels of potassium (K+).