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Do alterations in temperature regulation contribute to protein‐energy malnutrition‐induced increase in reactive gliosis after global ischemia?
Author(s) -
Smith Shari Elaine,
ProsserLoose Erin J,
Paterson Phyllis G
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.724.11
Subject(s) - hypothermia , ischemia , hyperthermia , medicine , gliosis , core temperature , anesthesia , endocrinology , brain ischemia , pathology
Protein‐energy malnutrition (PEM) impairs functional outcome after global ischemia, and this is associated with an increase in reactive gliosis. Since temperature is a key determinant of brain damage following an ischemic insult, the objective of this study was to determine if PEM modifies post‐ischemic temperature regulation. Bio‐electrical sensor transmitters were implanted into the peritoneal cavity of male, Sprague‐Dawley rats (31d) for continuous monitoring of core temperature. Rats were randomized for 7d to modified AIN‐93G control diet (CON; 18% protein) or PEM (2% protein). Animals were exposed to global ischemia (I) induced by 10 min bilateral carotid artery occlusion and hypotension (38 ± 0.2 mm Hg) or sham surgery (S) with tympanic temperature maintained at 37.4 ± 0.2°C. Physiological values were as follows: pH 7.29–7.41, pO 2 119–144 mm Hg, pCO 2 34–51 mm Hg, blood glucose 3.8–6.7 mmol/L. Preliminary results indicate mean (± SEM) core and daily temperature fluctuation from 5d of postsurgical monitoring as follows: CON‐S: 37.4 ± 0.04°C, 2.0 ± 0.1°C (n=3); PEM‐S: 37.4 ± 0.1°C, 2.6 ± 0.1°C (n=3); CON‐I: 37.7 ± 0.1°C, 1.9 ± 0.2 °C (n=3); PEM‐I: 37.5 ± 0.2°C, 2.3 ± 0.3°C (n=2). These data suggest that although PEM does not cause marked hypothermia or hyperthermia during the postsurgical period, it reduces thermoregulatory function in both sham and ischemic animals. Funded by the Heart and Stroke Foundation of SK.