Cardioplegia, CPD Cardioplegia, Blood Cardioplegia, Microplegia, Micro Cardioplegia, Myocardial Protection, Myocardial Protection Cardioplegia - Adenocaine and the Thermacor 1200 from Smisson-Cartledge Biomedical
Medical Research Article
Adenosine and Lidocaine: a New Concept in Non-Depolarizing Surgical Myocardial arrest, protection and preservation
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Adenosine and Lidocaine: a New Concept in Non-Depolarizing Surgical
Myocardial Arrest, Protection and Preservation
Geoffrey P Dobson PhD and Michael W. Jones BSc
Department of Physiology and Pharmacology,
James Cook University,
Townsville, Queensland,
Australia 4811
Key words: cardioplegia, adenosine, lidocaine, potassium, hyperkalemia, ATP-sensitive potassium channels
ABSTRACT
Objective: Depolarising potassium cardioplegia has been increasingly linked to left ventricular dysfunction, arrhythmias and microvascular damage. We tested a new polarising normokalemic cardioplegia employing adenosine and lidocaine (AL) as the arresting, protecting and preserving cardioprotective combination. Adenosine hyperpolarises the myocyte by A1 receptor activation, and lidocaine blocks the sodium fast channels.
Methods: Isolated-perfused rat hearts were switched from the working mode to the Langendorff (non-working) mode and arrested for 30 min, 2 or 4 hours with 200 ?M adenosine and 500 ?M lidocaine in Krebs-Henseleit buffer (10 mM glucose, pH 7.7 @ 37 °C) or modified St. Thomas’ Hospital solution No 2 both delivered at 70 mmHg and 37°C (arrest temperature 22-35°C).
Results: AL hearts achieved faster mechanical arrest in (25 ± 2 sec, n=23) compared to St. Thomas' hearts (70 ± 5 sec, n=24; P=.001)). After 30 min arrest, both groups developed comparable aortic flow at ~5 min of reperfusion. After 2 and 4 hours of arrest (cardioplegia delivered every 20 min for 2 min at 37°C), only 50% (4 out of 8) and 14% (1 out of 7) of St. Thomas’ hearts recovered aortic flow respectively. All AL hearts arrested for 2 hours (n=7) and 4 hours (n=9) recovered 70-80% of their pre-arrest aortic flows. Similarly, heart rate, systolic pressures and rate-pressure products to 85-100%, and coronary flows recovered to 70-80% pre-arrest values. Coronary vascular resistance during cardioplegia delivery was significantly lower (P<0.05) after 2 and 4 hours in hearts arrested with AL cardioplegia compared to hearts arrested with St. Thomas’ solution.
Conclusions: We conclude that AL polarising cardioplegia confers superior cardioprotection during arrest and recovery compared to hyperkalemic depolarising St. Thomas’ cardioplegia.
