Improved cardiac protection with Sabax cardioplegia in Langendorff isolated rat hearts

Open access


Objective: Cardioplegia is an important step to facilitate cardiac surgery while limiting intraoperative myocardial injury. Although recent advances in cardioplegic arrest methods have significantly contributed to better postoperative outcomes, there is still controversy regarding the optimal composition and temperature of the cardioplegic solution. Accordingly, we aimed to assess whether cold or lukewarm Sabax cardioplegia offer improved myocardial protection compared with the classical Krebs-Henseleit solution. Methods: The hearts of 40 male Wistar rats were isolated and submitted to constant-flow retrograde perfusion using a Langendorff perfusion apparatus. The hearts were randomly assigned to cold Krebs-Henseleit (K-H), cold Sabax, or lukewarm Sabax cardioplegia. The ECG, heart rates, and left ventricular systolic pressures (LVSP) were recorded pre- and post-cardioplegia. The time needed for cardioplegia induction and post-cardioplegia recovery were also noted. Results: Both cold and lukewarm Sabax cardioplegia insured faster induction and faster recovery following isothermic reperfusion compared to the standard K-H solution (both p< 0.01). With K-H cardioplegia, the hearts presented a 21.7% force loss after reperfusion (p< 0.001), whilst Sabax cardioplegia was associated with a slight increase in ventricular mechanical activity (3% LVSP increase with lukewarm Sabax cardioplegia, p< 0.001 and 2% LVSP increase with cold Sabax cardioplegia, p = 0.02). With Sabax cardioplegia the hearts displayed considerably less major arrhythmic events and presented less significant bradycardia. Conclusions: The present data suggest that Sabax cardioplegia may be superior to the classical cold crystalloid K-H solution in preserving mechanical activity of the heart and may provide superior protection against major arrhythmias.

If the inline PDF is not rendering correctly, you can download the PDF file here.

  • 1. Turer AT Hill JA. Pathogenesis of myocardial ischemia reperfusion injury and rationale for therapy. Am J Cardiol. 2010;106(3):360-368.

  • 2. Fremes SE Weisel RD Mickle DA et al. Myocardial metabolism and ventricular function following cold potassium cardioplegia. J Thorac Cardiovasc Surg. 1985;89:531-546.

  • 3. Fan Y Zhang AM Xiao YB Weng YG Hetzer R. Warm versus cold cardioplegia for heart surgery: a meta-analysis. Eur J Cardiothorac Surg. 2010;37(4):912-919.

  • 4. Kao YJ Mian T Kleinman S Racz GB. Hyperkalaemia: a complication of warm heart surgery. Can J Anaesth. 1993;40:67-70.

  • 5. Hickey E Karamlou T You J Ungerleider RM. Effects of circuit miniaturization in reducing inflammatory response to infant cardiopulmonary bypass by elimination of allogeneic blood products. Ann Thorac Surg. 2006;81:S2367-S2372.

  • 6. Ovrum E Tangen G Tollofsrud S et al. Cold blood versus cold crystalloid cardioplegia: a prospective randomized study of 345 aortic valve patients. Eur J Cardiothorac Surg. 2010;38:745-749.

  • 7. Minasian SM Galagudza MM Dmitriev YV Kurapeev DI Vlasov TD. Myocardial protection against global ischemia with Krebs-Henseleit bufferbased cardioplegic solution. J Cardiothorac Surg. 2013;8:60.

  • 8. Nakamura Y Taremoto N Kuroda H Ohgi S. The advantages of normocalcemic continuous warm cardioplegia over low calcemic cardioplegia in myocardial protection. Surg Today. 1999;29:884-889.

  • 9. Tevaearai HT Eckhart AD Shotwell KF Wilson K Koch WJ. Ventricular dysfunction after cardioplegic arrest is improved after myocardial gene transfer of a beta-adrenergic receptor kinase inhibitor. Circulation. 2001;104(17):2069-2074.

  • 10. Fukuhiro Y Wowk M Ou R Rosenfeldt F Pepe S.Cardioplegic strategies for calcium control: low Ca(2+) high Mg(2+) citrate or Na(+)/H(+) exchange inhibitor HOE-642. Circulation. 2000;102(19):III319-III325.

  • 11. Tang XN Yenari MA. Hypothermia as a cytoprotective strategy in ischemic tissue injury. Ageing Res Rev. 2010;9:61-68.

  • 12. Craver JM Bufkin BL Weintraub WS Guyton RA. Neurologic events after coronary bypass grafting: further observations with warm cardioplegia. Ann Thorac Surg. 1995;59(6):1429-1433.

  • 13. Tissier R Chenoune M Ghaleh B et al. The small chill: mild hypothermia for cardioprotection? Cardiovasc Res. 2010;88:406-414.

  • 14. Hale SL Kloner RA. Mild hypothermia as a cardioprotective approach for acute myocardial infarction: laboratory to clinical application. J Cardiovasc Pharmacol Ther. 2011;16:131-139.

  • 15. Sauer H Allen SJ Laine GA. Impact of crystalloid HTK and St. Thomas’ cardioplegia on myocardial fluid balance and postcardioplegic stunning. Cardiovasc Eng. 2003;8(1):58-65.

  • 16. Lochner A Lloyd L Brits W Coetzee A. Oxygenation of cardioplegic solutions: a note of caution. Ann Thorac Surg. 1991;51(5):777-787.

  • 17. The Warm Heart Investigators. Randomised trial of normothermic versus hypothermic coronary bypass surgery. Lancet. 1994;343(8897):559-563.

  • 18. Shaffer RF Baumgarten CM Damiano RJ Jr. Prevention of cellular edema directly caused by hypothermic cardioplegia: studies in isolated human and rabbit atrial myocytes. J Thorac Cardiovasc Surg. 1998;115(5):1189-1195.

  • 19. Haim SA Hayam G Edoute Y Better OS. Effect of hypertonicity on contractility of isolated working rat left ventricle. Cardiovasc Res. 1992;26(4):379-382.

  • 20. Buckberg GD Brazier JR Nelson RL et al. Studies on the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1977;73:87-94.

  • 21. Edelman JJ Seco M Dunne B et al. Custodiol for myocardial protection and preservation: a systematic review. Ann Cardiothorac Surg. 2013;2(6):717-728.

  • 22. Forman MB Puett DW Virmani R. Endothelial and myocardial injury during ischemia and reperfusion: pathogenesis and therapeutic implications. J Am Coll Cardiol. 1989;13(2):450-459.

Journal information
All Time Past Year Past 30 Days
Abstract Views 0 0 0
Full Text Views 204 141 11
PDF Downloads 85 70 5