Protein-energy malnutrition (PEM) has been found in up to 16.3% of acute stroke patients upon admission to hospital. Our laboratory has previously shown that PEM impairs functional outcome in a gerbil model of global ischemia, but the mechanism has not been established. The purpose of the current study was to characterize the marked reactive gliosis apparent in a subset of these animals that could represent an increased inflammatory response. A second objective was to validate a screening protocol for assessing completeness of ischemia in this model. Male Mongolian gerbils, aged 11-12 weeks, were randomized to PEM (2% protein) or control diet (12.5% protein) for 28d. PEM animals lost 12.2% of their initial body weight, and feed intake and serum albumin concentration were 12.3% and 17.8% lower than controls, respectively. At day 28, animals underwent 5 min bilateral common carotid artery occlusion (ischemia) or sham surgery. Activity was monitored using infrared beam interruptions for 20h post-surgery to screen for complete ischemia on the basis of persistent hyperactivity. Brain sections were stained with hematoxylin & eosin, and viable hippocampal CA1 neurons were counted at 10d post-ischemia. Immunohistochemistry for glial-fibrillary acidic protein (GFAP) and ricinus communis agglutinin -120 (RCA-120), markers for astrocytes and microglia, respectively, and the inflammatory cytokine TNF-alpha was performed on brain sections at 6h, 24h, 3d and 10d post-surgery (Ischemic, n=8; Sham, n=3). The activity monitoring procedure for detecting complete ischemia validated against hippocampal CA1 neuronal loss at 10d demonstrated an accuracy of 84.6%. Temporal changes in GFAP and RCA-120 immunoreactivity characteristic of reactive gliosis were demonstrated following ischemia, but this was not exacerbated by PEM. TNF-alpha immunoreactivity following ischemia was also unaltered by PEM. Ischemia significantly reduced surviving CA1 neurons at 10 days post-ischemia (two-way ANOVA; p<0.05), but this was not influenced by PEM. Impaired functional outcome in PEM animals following global ischemia can not be accounted for by increased hippocampal CA1 neuron death or by altered glial response.

Protein-energy malnutrition (PEM) has been found in up to 16.3% of acute stroke patients upon admission to hospital. Our laboratory has previously shown that PEM impairs functional outcome in a gerbil model of global ischemia, but the mechanism has not been established. The purpose of the current study was to characterize the marked reactive gliosis apparent in a subset of these animals that could represent an increased inflammatory response. A second objective was to validate a screening protocol for assessing completeness of ischemia in this model. Male Mongolian gerbils, aged 11-12 weeks, were randomized to PEM (2% protein) or control diet (12.5% protein) for 28d. PEM animals lost 12.2% of their initial body weight, and feed intake and serum albumin concentration were 12.3% and 17.8% lower than controls, respectively. At day 28, animals underwent 5 min bilateral common carotid artery occlusion (ischemia) or sham surgery. Activity was monitored using infrared beam interruptions for 20h post-surgery to screen for complete ischemia on the basis of persistent hyperactivity. Brain sections were stained with hematoxylin & eosin, and viable hippocampal CA1 neurons were counted at 10d post-ischemia. Immunohistochemistry for glial-fibrillary acidic protein (GFAP) and ricinus communis agglutinin -120 (RCA-120), markers for astrocytes and microglia, respectively, and the inflammatory cytokine TNF-alpha was performed on brain sections at 6h, 24h, 3d and 10d post-surgery (Ischemic, n=8; Sham, n=3). The activity monitoring procedure for detecting complete ischemia validated against hippocampal CA1 neuronal loss at 10d demonstrated an accuracy of 84.6%. Temporal changes in GFAP and RCA-120 immunoreactivity characteristic of reactive gliosis were demonstrated following ischemia, but this was not exacerbated by PEM. TNF-alpha immunoreactivity following ischemia was also unaltered by PEM. Ischemia significantly reduced surviving CA1 neurons at 10 days post-ischemia (two-way ANOVA; p<0.05), but this was not influenced by PEM. Impaired functional outcome in PEM animals following global ischemia can not be accounted for by increased hippocampal CA1 neuron death or by altered glial response.