Hyperglycemia Alters Expression of Cerebral Metabolic Genes after Cardiac Arrest.

Lindblom RPF, Molnar M, Israelsson C, Röjsäter B, Wiklund L, Lennmyr F

J Stroke Cerebrovasc Dis 27 (5) 1200-1211 [2018-05-00; online 2018-01-03]

Survivors of cardiac arrest often experience neurologic deficits. To date, treatment options are limited. Associated hyperglycemia is believed to further worsen the neurologic outcome. The aim with this study was to characterize expression pathways induced by hyperglycemia in conjunction with global brain ischemia. Pigs were randomized to high or normal glucose levels, as regulated by glucose and insulin infusions with target levels of 8.5-10 mM and 4-5.5 mM, respectively. The animals were subjected to 5-minute cardiac arrest followed by 8 minutes of cardiopulmonary resuscitation and direct-current shock to restore spontaneous circulation. Global expression profiling of the cortex using microarrays was performed in both groups. A total of 102 genes differed in expression at P < .001 between the hyperglycemic and the normoglycemic pigs. Several of the most strongly differentially regulated genes were involved in transport and metabolism of glucose. Functional clustering using bioinformatics tools revealed enrichment of multiple biological processes, including membrane processes, ion transport, and glycoproteins. Hyperglycemia during cardiac arrest leads to differential early gene expression compared with normoglycemia. The functional relevance of these expressional changes cannot be deduced from the current study; however, the identified candidates have been linked to neuroprotective mechanisms and constitute interesting targets for further studies.

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PubMed 29306595

DOI 10.1016/j.jstrokecerebrovasdis.2017.11.036

Crossref 10.1016/j.jstrokecerebrovasdis.2017.11.036

S1052-3057(17)30655-9