Normokalemic adenosine-lidocaine cardioplegia: importance of maintaining a polarized myocardium for optimal arrest and reanimation.
OBJECTIVE
Depolarizing potassium cardioplegia does not afford optimal cardioprotection in pediatric or adult patients requiring complicated operative procedures. Polarizing adenosine-lidocaine cardioplegia has been shown to be cardioprotective without hyperkalemia. Our aim was to examine the effects of changing extracellular potassium levels in adenosine-lidocaine cardioplegia on arrest and reanimation properties.


METHODS
Isolated-perfused rat hearts (n = 96) were arrested at 32 degrees C to 33 degrees C for 1 or 2 hours with intermittent 200 mumol/L adenosine and 500 mumol/L lidocaine in modified Krebs-Henseleit buffer with 0.1, 3.0, 5.9, 10, and 16 mmol/L potassium or with 16 or 25 mmol/L potassium in Krebs-Henseleit buffer (n = 8 for each group). Membrane potentials were estimated in the arrested ventricular myocardium (n = 42), and recovery function was measured in working mode during 60 minutes' reperfusion.


RESULTS
Arrest was interrupted by breakout beats in the adenosine-lidocaine hypokalemic (0.1 and 3 mmol/L potassium) and non-adenosine-lidocaine hyperkalemic (16 and 25 mmol/L potassium) groups. The membrane potentials for the non-adenosine-lidocaine 16 and 25 mmol/L potassium groups were -51 and -39 mV, and those for the adenosine-lidocaine groups (0.1, 3.0, 5.9, 10, and 16 mmol/L potassium) were -183, -94, -75, -65, and -49 mV, respectively. After 1 hour of arrest, coronary vascular resistance increased linearly in adenosine-lidocaine cardioplegia with increasing potassium levels (5.9, 10, and 16 mmol/L), and the slope increased more than 2-fold after 2 hours. Nearly 40% of hearts in the adenosine-lidocaine (0.1 mmol/L potassium) and non-adenosine-lidocaine 25 mmol/L potassium groups failed to recover after 1 hour arrest. After 2 hours, hearts in the polarizing (5.9 mmol/L potassium) adenosine-lidocaine group increased coronary vascular resistance 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 minutes) with no reperfusion arrhythmias. In contrast, hearts in the adenosine-lidocaine (3, 10, and 16 mmol/L potassium) groups were all slow to recover (15% to 40% return at 15 minutes) and experienced arrhythmias. Increasing potassium levels in adenosine-lidocaine cardioplegia from 5.9 to 16 mmol/L resulted in a 67% loss of left ventricular contractility.


CONCLUSIONS
Polarizing adenosine-lidocaine cardioplegia (5.9 mmol/L potassium) administered intermittently at 33 degrees C provides superior arrest and reanimation profiles under normokalemic conditions when the myocardial cell membrane potential is close to its resting state.
Sloots
Kathryn L
KL
Heart Research Laboratory, Department of Physiology and Pharmacology, Molecular Science Building, James Cook University, Townsville, Queensland 4811, Australia.
Dobson
Geoffrey P
GP
D000241:Adenosine / Q000008:administration & dosage*; D000818:Animals; D045604:Extracellular Fluid / Q000737:chemistry; D006321:Heart / Q000502:physiology*; D006324:Heart Arrest, Induced / Q000379:methods*; D066298:In Vitro Techniques; D008012:Lidocaine / Q000008:administration & dosage*; D008297:Male; D008564:Membrane Potentials; D011188:Potassium / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation
D008012:Lidocaine; D000241:Adenosine; D011188:Potassium