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Ann Thorac Surg 1997;63:449-454
© 1997 The Society of Thoracic Surgeons

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Original Article: Cardiovascular

Functional and Metabolic Effects of Adenosine in Cardioplegia: Role of Temperature and Concentration

Heart Science Centre, National Heart and Lung Institute at Harefield Hospital, Harefield, Middlesex, United Kingdom

Accepted for publication August 31, 1996.

Background. Addition of adenosine to cardioplegic fluid has been shown to improve myocardial tolerance to ischemia. This study was designed to investigate further this phenomenon to evaluate the dose-response and the temperature dependence of the effect of addition of adenosine to St. Thomas' Hospital cardioplegic solution.

Methods. The isolated working rat heart model was used in this study. After the assessment of control function, hearts (6 in each group) were subjected to infusions of cardioplegic solution containing 0.0 (control), 0.1, 5.0, 10.0 or 20.0 mmol/L adenosine followed by 3 hours of ischemic arrest at temperatures of 20°C, 10°C, or 4°C with multidose (3 minutes every 30 minutes) cardioplegic infusion.

Results. After ischemic arrest at 20°C, the recovery of cardiac output (expressed as percent of preischemic baseline) was 35.4 ± 5.11 (control) 45.0 ± 5.51 (0.1 mmol/L), 53.1 ± 2.9 (5.0 mmol/L), 61.8 ± 3.7 (10.0 mmol/L), and 57.6 ± 2.3 (20.0 mmol/L). Hearts receiving 5.0 to 20.0 mmol/L adenosine had significantly greater recovery of cardiac output than control hearts. In its optimal concentration (10 mmol/L), adenosine improved the efficacy of the cardioplegic solution by almost 75%. Myocardial adenosine triphosphate content (expressed in µmol/g protein) was 4.7 ± 0.5 (control), 4.9 ± 1.4 (0.1 mmol/L), 8.1 ± 0.7 (5 mmol/L), 12.5 ± 2.0 (10 mmol/L), and 11.2 ± 2.8 (20 mmol/L), at the end of ischemia and 13.9 ± 0.2 (control), 13.1 ± 1.7 (0.1 mmol/L), 18.0 ± 2.0 (5 mmol/L), 18.6 ± 1.2 (10 mmol/L), and 20.7 ± 2.1 (20 mmol/L) at the end of reperfusion. Thus, the adenosine triphosphate content was higher (p < 0.05) in hearts receiving 5.0 to 20.0 mmol/L adenosine than in controls both at the end of ischemia and after reperfusion. Myocardial adenosine monophosphate level at the end of ischemia was inversely related to adenosine triphosphate level. Functional assessment of the effect of 10 mmol/L adenosine at 10°C and 4°C during arrest indicated attenuation of beneficial effects: adenosine improved function only by 17% at 10°C, whereas at 4°C the protective effect was not observed.

Conclusions. These observations suggest that adenosine has the potential to enhance the efficacy of clinical cardioplegic arrest but the degree of improvement is lower at decreased temperature during ischemia. A principal mechanism of action of this modification of cardioplegic fluid appears to be through the inhibition of high-energy phosphate utilization immediately before or during ischemia.

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Invited Commentary

Steven F. Bolling
Ann. Thorac. Surg. 1997 63: 454-455. [Extract] [Full Text]

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