• Xingmin Wang, Rui Song, Yunyan Chen, Ming Zhao, and Ke-seng Zhao.
• Southern Medical University, Department of Pathophysiology, Guangdong Key Laboratory of Shock and Microcirculation Research, Guangzhou, PR China.
• Expert Opin Investig Drugs. 2013 Feb 1;22(2):169-79.

ObjectiveThe aim of the study was find out whether neuronal mitochondrial injury does take place in severe shock and to explore effective therapy for severe shock.Research Design And MethodsRats were divided in the following group: sham, shock + normal saline (NS), shock + cyclosporine A (CsA), shock + resveratrol (Res) and shock + polydatin (PD). Rats were subjected to shock for 2 h, followed by administration of NS, CsA, Res and PD, and infusion of shed blood. Morphology, metabolism and function of mitochondria were measured.ResultsIncreased lipid peroxides (LPO) levels, lysosomal injury and mitochondrial permeability transition pore opening took place in neurons, resulting in swollen mitochondria with poorly defined cristae, decreased mitochondrial membrane potential (ΔΨ) and reduced ATP content in shock + NS group, indicating mitochondrial dysfunction. Mitochondrial protectors, such as CsA, Res and PD, partially inhibited these alterations, especially following PD protection, ATP level increased from 44.14 ± 13.81% in shock + NS group to 89.57 ± 9.21% and the survival time was prolonged from 6.3 ± 5.9 h in the shock + NS group to 31.6 ± 13.7 h in shock + PD group.ConclusionsThe study shows that neuronal mitochondrial injury is involved in the genesis of severe shock and PD may be the best choice for protection of neuron against mitochondrial injury in severe shock.

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