Uniformed Services University of the Health Sciences F. Edward Hebert School of Medicine Biomedical Graduate Programs

نویسندگان

  • Joseph O'Sullivan
  • Joseph C. O'Sullivan
  • Joseph C. O’Sullivan
چکیده

Our team tested the hypothesis that pharmacological induction of ischemicpreconditioning can offer cytoprotection and preserve vital tissues after hemorrhagicshock and stroke. The compound, diazoxide (DZ), is known to induce preconditioningthrough its effect as a mitochondrial KATP channel opener and succinate dehydrogenaseinhibitor. When DZ was administered 24 hours prior to shock, it significantly reducedhyperglycemia, which in vehicle-treated animals persisted after resuscitation. DZ alsoattenuated hyperlactatemia during the 1 hour shock period. With more severe traumafrom combined shock and stroke, DZ also decreased hyperlactatemia and hyperglycemialevels but the reduction was only significant for hyperglycemia. DZ also seems toincrease the survival rate of animals that sustained combined stroke and shock, but not significantly (p=.058). The expression levels of heat shock proteins 25 (HSP25) and 70(HSP70) were used as biomarkers for response of the kidney and liver to DZ andcombined stroke and shock. Compared to vehicle-treated animals, DZ-treated ratssubjected to shock and stroke exhibited increased HSP25 and HSP70 in kidney and livertissue. Taken together, these results suggest DZ attenuates physiological indicators ofmetabolic stress following shock or combined shock and stroke, that it may increase

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Preconditioning and Postconditioning

Joseph T. McCabe1, Michael W. Bentley2 and Joseph C. O’Sullivan2 1Department of Anatomy, Physiology & Genetics, and The Center for Neuroscience & Regenerative Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 2U.S. Army Graduate School of Anesthesia Nursing, Graduate School, AMEDD Center and School, Academy of Health Sciences, Fort Sam Houston, San Antonio, Texa...

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تاریخ انتشار 2008