Comparison of the effects of cyclosporin A on the metabolism of perfused rat brain slices during normoxia and hypoxia
Comparison of the effects of cyclosporin A on the metabolism of perfused rat brain slices during normoxia and hypoxia
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DOI:
10.1097/00004647-200203000-00012
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发表时间:
2002-03-01
影响因子:
6.3
通讯作者:
Christians, U
中科院分区:
文献类型:
--
作者:
Serkova, N;Donohoe, P;Christians, U
The authors evaluated and compared the metabolic effects of cyclosporin A in the rat brain during normoxia and hypoxia/reperfusion. Ex vivo P-31 magnetic resonance spectroscopy experiments based on perfused rat brain slices showed that under normoxic conditions, 500 mug/L cyclosporin A significantly reduced mitochondrial energy metabolism (nucleotide triphosphate, 83 +/- 9% of controls; phosphocreatine, 69 +/- 9%) by inhibition of the Krebs cycle (glutamate, 77 +/- 5%) and oxidative phosphorylation (NAD(+), 65 +/- 14%) associated with an increased generation of reactive oxygen species (285 +/- 78% of control). However, the same cyclosporin A concentration (500 mug/L) was found to be the most efficient concentration to inhibit the hypoxia-induced mitochondrial release of Ca2+ in primary rat hippocampal cells with cytosolic Ca2+ concentrations not significantly different from normoxic controls. Addition of 500 mug/L cyclosporin A to the perfusion medium protected high-energy phosphate metabolism (nucleotide triphosphate, 11 +/- 15% of control vs. 35 +/- 9% with 500 mug/L cyclosporin A) and the intracellular pH (6.2 +/- 0.1 control vs. 6.6 +/- 0.1 with cyclosporin A) in rat brain slices during 30 minutes of hypoxia, Results indicate that cyclosporin A simultaneously decreases and protects cell glucose and energy metabolism. Whether the overall effect was a reduction or protection of cell energy metabolism depended on the concentrations of both oxygen and cyclosporin A in the buffer solution.