1. Adenosine Prevents Hyperkalemia-Induced Calcium Loading in Cardiac Cells: Relevance for Cardioplegia 
Aleksander Jovanović, MD, Alexey E Alekseev, PhD, Jóse R López, MD, Win K Shen, MD, Andre Terzic, MD 
The Annals of Thoracic Surgery 
Volume 63, Issue 1, Pages (January 1997)
DOI: /S (96)

2. Fig. 1
Elevation of extracellular K+ induces intracellular Ca2+ loading in single ventricular cardiomyocytes. (A) Epifluorescent images from a Fluo-3 acetoxylmethyl ester (Fluo-3AM)–loaded cardiomyocyte prior to (frame 1) and after the (frame 2) addition of 16 mmol/L K+ to the solution bathing the myocyte. White horizontal bar indicates 20 μm. (A1) Changes in intensity of Fluo-3AM fluorescence plotted as a function of time from myocyte in Fig. 1. Circles labeled 1 and 2 correspond to frames 1 and 2. (B) Average changes in maximal fluorescence under control conditions, and after addition of 16 mmol/L K+. Each bar represents the mean ± the standard error of the mean (∗ = p < 0.01 between the two means.)
The Annals of Thoracic Surgery  , DOI: ( /S (96) )

3. Fig. 2
Adenosine prevents K+-induced Ca2+ loading. (A) Epifluorescent images from a cardiomyocyte under control conditions (frame 1), in adenosine (frame 2), in adenosine plus 16 mmol/L K+ (frame 3), and in 16 mmol/L K+ only (frame 4). White horizontal bar indicates 20 μm. (A1) Changes in intensity of Fluo-3 acetoxymethyl ester (Fluo-3AM) fluorescence plotted as a function of time from myocyte in Fig. 2. Circles labeled 1 through 4 correspond to frames 1 through 4. Adenosine alone did not significantly change the Fluo-3AM fluorescence, yet it prevented 16 mmol/L K+ to induce Ca2+ loading. (B) Average changes in maximal fluorescence under control conditions, in adenosine, in adenosine plus 16 mmol/L K+, and in 16 mmol/L K+ only. Each bar represents the mean ± the standard error of the mean. (∗ = p < 0.01 compared with control.)
The Annals of Thoracic Surgery  , DOI: ( /S (96) )

4. Fig. 3
Staurosporine, but not glyburide, antagonizes action of adenosine against K+-induced Ca2+ loading. Epifluorescent images from (A) glyburide-pretreated cardiomyocyte and (B) staurosporine-pretreated cardiomyocyte under control conditions (frame 1), in adenosine (frame 2), in adenosine plus 16 mmol/L K+ (frame 3), and in 16 mmol/L K+ (frame 4) and corresponding graph showing changes in intensity of Fluo-3 acetoxylmethyl ester fluorescence as a function of time. Circles labeled 1 through 4 correspond to frames 1 through 4. Glyburide (3 μmol/L) or staurosporine (200 nmol/L) was continuously present throughout the experiment. White horizontal bar indicates 20 μm, and corresponding graph. (C) Average changes in maximal fluorescence under control conditions, in adenosine, in adenosine plus 16 mmol/L K+, and in 16 mmol/L K+ in glyburide-pretreated (n = 6) or in staurosporine-pretreated (n = 4) cardiomyocytes. Each bar represents the mean ± the standard error of the mean. (∗ = p < 0.01) compared with respective controls.)
The Annals of Thoracic Surgery  , DOI: ( /S (96) )

5. Fig. 4
Chelerythrine, an inhibitor of protein kinase C, antagonizes the action of adenosine against K+-induced Ca2+ loading. (A) Epifluorescent images from adenosine-treated cardiomyocyte challenged with 16 mmol/L K+ before (frame 2) and after (frames 5 and 6) treatment with chelerythrine. White horizontal bar indicates 20 μm. (A1) Corresponding graph showing changes in intensity of Fluo-3 acetoxylmethyl ester fluorescence as a function of time. Circles labeled 1 through 6 correspond to frames 1 through 6. (B) Average changes in maximal fluorescence in chelerythrine-pretreated cardiomyocytes (n = 8) in adenosine and in adenosine plus 16 mmol/L K+. Each bar represents the mean ± the standard error of the mean. (arb. = arbitrary; ∗ = p < 0.01 compared with adenosine alone.)
The Annals of Thoracic Surgery  , DOI: ( /S (96) )