The effect of fructose-1,6-diphosphate and HTK solution on protecting primary cardiac muscle cells of rat with cold preservation

Abstract

In this study we tried to investigate the effect of fructose-1,6-diphosphate and HTK solution on protecting primary cardiac muscle cells of rat with cold preservation. The primary cardiac muscle cells of rat were cultured in vitro with four preservation solutions respectively: 0.9% sodium chloride solution (group A), FDP (group B), HTK solution (group C) and a mixture of FDP and HTK solution (group D). The cells were preserved for 6, 8 and 10 h at 0–4°C. The values of AST and LDH-L and the Na⁺-K⁺ ATPase activity in cardiac muscle cells were detected, and the survival rate of cardiac muscle cells was detected with trypan blue staining. The values of AST and LDH-L in group C and group D were remarkable lower those in group A and group B (P<0.001), while the Na⁺-K⁺ ATPase activity and the survival rate of cells in group C and group D were much higher than those in group A and group B (P<0.001). The values of AST and LDH-L after 6 hours in group D decreased much more than those in group C (P<0.01), while the Na⁺-K⁺ ATPase activity and the survival rate of cells in group D improved more than those in group C (P<0.01). Both of the HTK solution and the mixture of HTK and FDP solution have an evident effect on protecting the primary cardiac muscle cells of rat in vitro with cold preservation, Compared with the HTK solution, the mixture solution has a better short-term protective effect.

Keywords

fructose-1,6-diphosphate (FDP) / HTK solution / primary cardiac muscle cells

References

[1] WilsonC H, StansbyG, HaswellM, et al.. Evaluation of eight preservation solution for endothelial in situ preservation. Transplantation, 2004, 78(7): 1008-1008

[2] BelzerF O, SouthardJ H. Principles of solid-organ preservation by coldstorage. Transplanstation, 1988, 45(4): 673-673

[3] SanoW, WatanabeF, TamaiH, et al.. Beneficial effect of fructose-1,6-disphosphate on mitochondrial function during ischemia-reperfusion of rat liver. Gastroenterology, 1995, 08(6): 1785-1785

[4] SolaA, AlfaroV, PesqueroJ, et al.. CO2 in static mesenteric venous blood during intestinal ischemia and ischemic preconditioning in rats. Shock, 2001, 16(5): 403-403

[5] XiaoL, LuR, HuC P, et al.. Delayed cardioprotection by intestinal preconditioning is mediated by calcitonin generelated peptide. Eur J Pharmacol, 2001, 427(2): 131-131

[6] SunZ, WangX, DengX, et al.. Beneficial effects of lexipafant, a PAF antagonist on gut barrier dysfunction caused by intestinal ischemia and reperfusion in rats. Dig Surg, 2000, 17(1): 57-57