Figures & data
Figure 1. Time changes of left ventricular developed pressure (LVDP) (% of equilibrium values) during 60 min of reperfusion after hypothermic preservation. (A) 3 h of preservation; (B) 8 h of preservation. Data are expressed as mean ± SD, n = 8. *p < 0.05, **p < 0.01 vs. control group; #p < 0.05, ##p < 0.01 vs. 30 μM DE group; +p < 0.05, ++p < 0.01 vs. 15 μM DE group.
Figure 2. Recovery of coronary flow (CF) (% of equilibrium values) at the end of reperfusion after hypothermic preservation. Data are expressed as mean ± SD, n = 8. *p < 0.05, **p < 0.01 vs. control group; #p < 0.05, +p < 0.05 vs. 15 μM DE group.
Figure 3. Release of myocardial lactate dehydrogenase (LDH) in coronary effluent before arrest and during reperfusion after hypothermic preservation. (A) 3 h of preservation; (B) 8 h of preservation. Data are expressed as mean ± SD, n = 8. *p < 0.05, **p < 0.01 vs. control group; ##p < 0.01 vs. 30 μM DE group.
Figure 4. Release of myocardial creatine kinase (CK) in coronary effluent before arrest and at the 4th min of reperfusion after hypothermic preservation. Data are expressed as mean ± SD, n = 8. *p < 0.05, **p < 0.01 vs. control group; #p < 0.05, ##p < 0.01 vs. 30 μM DE group.
Figure 5. Evaluation of cardiomyocyte apoptosis using terminal dUTP nick-end labeling (TUNEL) after 8 h of hypothermic preservation. Data are expressed as mean ± SD, n = 7–8. *p < 0.05 vs. control group; #p < 0.05 vs. 30 μM DE group.
Figure 6. Cardiomyocyte apoptosis detected by TUNEL after 8 h hypothermic preservation (×200). Brown staining (TUNEL positive) indicates apoptotic cardiomyocytes (arrow). (A) Normal group: myocardium simply perfused with K–H solution for 30 min; (B) control group: myocardium preserved in Celsior solution for 8 h; (C) DE group: myocardium preserved in Celsior solution supplemented with 30 μM DE for 8 h; (D) 5-HD + DE group: myocardium preserved in Celsior solution supplemented with 30 μM DE and 100 μM 5-HD for 8 h.
Figure 7. Activities of mitochondrial superoxide dismutase (SOD) in preserved hearts and reperfused hearts. Data are expressed as mean ± SD, n = 8. **p < 0.01 vs. control group; #p < 0.05 vs. 30 μM DE group.Compared with the control, the 30 μM DE addition could significantly inhibit the rise in cardiomyocyte mitochondrial MDA level after 8 h in vitro hypothermic ischemic preservation and 8 h ischemic preservation plus 30 min reperfusion (p < 0.05). The 5-HD + DE group showed no significant difference compared with the control (p > 0.05) ().
Figure 8. Changes of mitochondrial malondialdehyde (MDA) in preserved hearts and reperfused hearts. Data are expressed as mean ± SD, n = 8. *p < 0.05, **p < 0.01 vs. control group; #p < 0.05, ##p < 0.01 vs. 30 μM DE group.
