Figure 7.

Influence of modified Krebs-Henseleit buffers on cold-induced injury of hepatocytes and aortic endothelial cells. Rat hepatocytes (A; n = 5) and porcine aortic endothelial cells (B; n = 4) were incubated in Krebs-Henseleit buffer with (KHG) or without (KH) glucose and modified Ca2+ and Pi concentrations for 14 h (rat hepatocytes) or 24 h (endothelial cells) at 4°C. Calcium concentrations in modified buffers were reduced (Ca-, 0.42 mM) or calcium was nominally absent (Ca--), Pi concentrations were increased in two steps (P+, 5.6 mM; P++, 25 mM). To part of the incubations, deferoxamine (+ Def.; 1 mM) or trifluoperazine (tfp; 20 μM) plus fructose (10 mM) were added. Ethanol served as solvent control for tfp (+ EtOH). Cell injury directly after cold storage (rat hepatocytes: 14 h, porcine aortic endothelial cells: 24 h) was assessed by release of lactate dehydrogenase (LDH; A: * = significantly different from KHG, + = significantly different from KHG(Ca--/P++); B: * = significantly different from KHG(Ca--,P++)).

Pless-Petig et al. BMC Biotechnology 2012 12:73   doi:10.1186/1472-6750-12-73
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