Cardioplegia, CPD Cardioplegia, Blood Cardioplegia, Microplegia, Micro Cardioplegia, Myocardial Protection, Myocardial Protection Cardioplegia - Adenocaine and the Thermacor 1200 from Smisson-Cartledge Biomedical

Toward a new cold and warm nondepolarizing, normokalemic arrest paradigm for orthotopic heart transplantation

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Authors:   Donna M. Rudd, MSc, and Geoffrey P. Dobson, PhD

Objective:  Currently, the safe human heart preservation time is limited to around 4 to 5 hours of cold ischemic storage. Longer arrest times can lead to donor heart damage, early graft dysfunction, and chronic rejection. The aim of this study was to examine a new nondepolarizing, normokalemic preservation solution with adenosine and lidocaine for as long as 6 hours of arrest at cold and warmer storage temperatures.

Methods:  Isolated perfused rat hearts (n ¼ 87) were switched from working to Langendorff (nonworking) mode and arrested at 37C with 200-mmol/L adenosine and 500-mmol/L lidocaine in Krebs–Henseleit buffer (10-mmol/ L glucose, pH 7.7, 37C) or with Celsior (Sangstat Medical Corp, Fremont, CA). Hearts were removed and placed in static storage at 4C for 2 and 6 hours or remained on the apparatus and were intermittently flushed at 37C every 20 minutes for 2 minutes at 68 mm Hg (average arrest temperature 28–30C) for 2 and 6 hours. We further investigated the effect of the warmer adenosine–lidocaine solution supplemented with 1- or 5-mmol/L pyruvate.
 

Results:  Adenosine–lidocaine solution arrested hearts in 16 +/- 2 seconds (n = 32), whereas Celsior did so in 39 +/- 4 seconds (n = 23). After 2 hours of cold static storage, there were no functional differences between the adenosine– lidocaine and Celsior groups, with approximately 70% return of cardiac output. In contrast, after 6 hours of 4C storage, adenosine–lidocaine hearts had significantly higher functional recoveries (68% +/- 5% cardiac output) than Celsior hearts (47%+/-14%cardiac output) during 60 minutes of reperfusion. In addition, Celsior hearts took 5 minutes longer to reanimate and showed early reperfusion arrhythmias. At warmer temperatures after 2 hours of arrest, adenosine–lidocaine and Celsior hearts were not significantly different, despite a 43% higher cardiac output in adenosine–lidocaine hearts (80% +/- 3% vs 56% +/- 12%). After 6 hours, adenosine–lidocaine hearts had recovered 55% +/- 3% of prearrest cardiac output, which increased significantly to 75% +/- 4% with addition of 1-mmol/L pyruvate. Adenosine– lidocaine with 1-mmol/L pyruvate hearts spontaneously recovered 106% heart rate, 93% to 105% developed pressures, 70% aortic flow, and 81% coronary flow. Coronary vascular resistance increased 1.7- to 1.9-fold during the 6-hour arrest. In contrast, Celsior hearts did not have return of aortic or coronary flow after 6 hours in these warmer conditions.

Conclusion:  A new nondepolarizing, normokalemic adenosine–lidocaine arrest solution in Krebs–Henseleit buffer with 10-mmol/L glucose was versatile at both 4C and 28C to 30C relative to Celsior, and the addition of 1-mmol/L pyruvate significantly improved cardiac output at warmer arrest temperatures. This new arrest paradigm may be useful in the harvest, storage, and implantation of donor hearts.