Plasma FN concentrations are decreased in Reye's Syndrome. FN depletion in experimental animals potentiates the systemic effects of EN. The purpose of this study was to determine the effect of FN depletion on the response to endotoxin. Sprague-Dawley male rats (n=30) were entered into 4 groups: (C) Control (D5W IV), (F) FN depletion (1% gelatin 15 mg/kg IV), (E) E. coli EN (0.2 mg/kg IP), and (FE) 1% gelatin (15 mg/kg IV) followed in one hour with EN (0.2 mg/kg IP). Serum ammonia (NH3), free fatty acids (FFA), lactate, glucose, SGOT and SGPT were obtained prior to fasting (baseline), 12 hours after onset of fast, and upon sacrifice (12 hr after test injection). At sacrifice, liver, spleen and brain specimens were fixed for fat staining, routine histology, and electron microscopy (EM). Plasma chemistry values were unchanged by fasting.
FE resulted in significant increases in NH3 and FFA over control (p<.05*). FE and E revealed increased microvesicular hepatic fat (without necrosis) compared to fasting controls. EM demonstrated loss of cristae and matrix disruption in hepatic and splenic but not brain mitochrondria. SGOT, SGPT, and serum glucose were unchanged from baseline levels in all groups. Thus, FN depletion and EN administration produces metabolic, histologic, and ultrastructural changes similar to Reye's Syndrome.
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Yoder, M., Yudkoff, M., Chatten, J. et al. LOW DOSE ENDOTOXIN (EN) AND FIBRONECTIN (FN) DEPLETION IN RATS: A MODEL OF REYE'S SYNDROME. Pediatr Res 18, 289 (1984) doi:10.1203/00006450-198404001-01176
The Journal of Pediatrics (1984)