Summary:We investigated metabolic changes in human umbilical venous endothelial cells, when these were incubated under hypoxic followed by hyperoxic conditions, thus simulating hypoxia and reoxygenation..The human umbilical venous endothelial cells were incubated with a degassed buffer (oxygen content: 0-0.5%) for either 3 h or 24h, followed by a 60min incubation with oxygen-perfused buffer (oxygen content: 100%). Three hours of hypoxia led to a slight decrease in the ATP and creatine phosphate content (-16% ± 5%), while a pronounced decrease of high energy phosphates (-54% ± 4%) was observed after 24 h of hypoxia. Reoxygenating the cells after 3 h of hypoxia led to restoration of the content of high energy phosphates, while reoxygenation after 24 h resulted in a strong decrease (-66% ± 4%). The prostaglandin I 2 release during the first 3 h of hypoxia exceeded the release in the following 21 h. In all cases, reoxygenation increased the prostaglandin I 2 release. Under normoxic conditions the ratio between oxidised glutathione and reduced glutathione shifted from l : 100 to l : 4.5 after 3 h of hypoxia. The content of lipid peroxidation products was almost unaffected during hypoxia, whereas reoxygenation resulted in a pronounced increase (+ 380% ± 60%). The results of this in vitro study suggest that relatively long periods of hypoxia lead to a deficiency of high energy phosphates in the cell. Reoxygenation leads to the formation of oxygen-derived radicals, irrespectively of a prior hypoxia.

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In the present study the effect of oxygenated Bretschneider cardioplegia on high-energy phosphates [adenosine triphos-phate (ATP), adenosine diphosphate (ADP) and creatine phosphate (CP)] and hemodynamics was evaluated in the isolated working rabbit heart. Hearts were obtained from 37 adult white Elco rabbits (3,100 ± 110 g). After a 20-min working period 14 hearts were arrested with Bretschneider cardioplegia (8 °C) oxygenated with 98% oxygen (O₂) and 2% carbon dioxide in comparison to 14 hearts receiving Bretschneider solution saturated with 98% nitrogen (N₂) and 2% carbon dioxide as a control group for either 60 or 90 min (O₂6O, O₂90, N₂60, N₂90 groups, n = 7). Seven hearts were used to determine preischemic baseline values of ATP, ADP and CP, 2 were excluded. The results showed a significantly poorer preservation of high-energy phosphates in hearts receiving oxygenated Bretschneider cardioplegia as compared to hearts receiving nitrogenated cardioplegia (p < 0.05). Postischemic recovery of hemodynamics did not demonstrate any statistically significant differences between the groups. However, the intragroup analysis showed a tendency towards weaker hemodynamic recovery in hearts treated with oxygenated cardioplegia. These results stay in contrast to the beneficial effect of oxygenated St. Thomas solution. In conclusion our findings suggest that oxygenated Bretschneider cardioplegia leads to significantly poorer preservation of high-energy phosphates and depressed hemodynamic recovery.

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