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Ann Thorac Surg 2001;72:1447-1448
© 2001 The Society of Thoracic Surgeons
a Division of Cardiovascular Surgery, University of Pittsburgh Medical Center, Shadyside Hospital, 5200 Centre Ave, Suite 216, Pittsburgh, PA 15232, USA
To the Editor
Myocardial arrest is achieved during standard cardiac surgical procedures by administering potassium cardioplegic solution. This causes depolarized myocardial arrest. While this is very effective, depolarization at the cell membrane leads to ionic exchange, increase in intracellular calcium, and depletion of energy substrates. To minimize these adverse effects, polarized or hyperpolarized arrests are being investigated and the common chemical agent that has been examined is adenosine. Adenosine is an autacoid produced by the myocytes and has an effect on various receptors of the cell membrane. It has a vasodilator effect and achieves hyperpolarized arrest by decreasing the membrane potential up to -120 millivolts. At this level, ionic exchange does not occur and myocardial arrest is achieved without energy expenditure. This has been the mechanism of adenosine action and its effect on ischemic preconditioning of the myocardium. This has been studied by several surgeons in an experimental model. Clinically, it has been administered during off-pump coronary artery bypass to slow down the beating heart and also to gain the benefit of minimizing myocardial ischemia. Lee and associates [1] have reported administering 250 to 350 mcg/kg adenosine prior to going on cardiopulmonary bypass.
Adenosine is also considered to have severe neutrophil inhibitory effect and blocking of neutrophil endothelial cell interaction [2]. While this effect is studied in the myocardium to limit the infarct size and to improve myocardial functional recovery, this may be more general than isolated in the myocardium alone. Institution of cardiopulmonary bypass alone activates complement as well as neutrophils. The inflammatory response can cause fluid retention and can cause various organ dysfunctions including that of the brain and lungs. Before we can randomize patients to compare the advantage of adenosine, we have administered 12 mg of adenosine intravenously 2 to 3 minutes before going on cardiopulmonary bypass, and 12 mg into the initial cardioplegic administration for hyperpolarized arrest. This has been done in more than 100 patients. The results are impressive. While the myocardial functional recovery is better in all subgroups of patients with simple or complicated surgical procedures, we are pleasantly surprised about the lack of neurological complications even in octogenarians. Cerebral dysfunction, mental confusion, and loss of memory that were seen in some subgroups of patients in the past have been consistently absent in the adenosine group. While we continue to use this drug in routine cardiac surgery, we are looking for scientific studies that can help us elucidate the knowledge that adenosine, by inhibiting neutrophil activity, may also have some cerebro-protective effects.
References
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