The peri-microvascular edema in hippocampal CA1 area in a rat model of sepsis

Abstract

Neuropathology 2007; 27, 213–220 doi:10.1111/j.1440-1789.2007.00757.x © 2007 Japanese Society of Neuropathology Original Article The peri-microvascular edema in hippocampal CA1 area in a rat model of sepsis Ilker Mustafa Kafa, Ilknur Ari and Mustafa Ayberk Kurt Uludag University, Faculty of Medicine, Anatomy Department, Bursa, Turkey Encephalopathy is a common complication of sepsis. How- ever, little is known about the morphological changes that occur in the brain during sepsis. In this study, fecal perito- nitis was induced in Wistar rats, which had been monitored for 4 h before their brains were removed and samples from the CA1 area taken. In addition to higher blood pressure with a decreasing pattern and a significant drop in rectal temperature, an increased heart rate and marked respira- tory failure were observed. The tissue was investigated and compared with corresponding hippocampal samples taken from sham-operated and not operated control groups. Sig- nificantly more peri-microvascular edema was found in the hippocampal CA1 area in the septic group. The percent- ages of the peri-microvascular edema were 158.57 ± 3.6%, 122.84 ± 1.5% and 120.24 ± 1.9% in the fecal peritonitis group, sham-operated and not operated control groups, respectively. The results may suggest that the edema observed around the microvessels may participate in the pathogenesis of the septic encephalopathy probably by causing in the microvascular permeability characteristics. Key words: CA1, fecal peritonitis, hippocampus, peri- microvascular edema, septic encephalopathy. INTRODUCTION Septic shock is the commonest cause of death in intensive care units. Sepsis and septic shock is associated with widespread endothelial cell damage caused by persistent, uncontrolled inflammation.1,2 Damage to vascular endot- helium caused by infectious agents triggers the release of a variety of mediators of inflammation. Uncontrolled inflam- mation causes the deposition of fibrin and the formation of thrombi in

Part of CIRS Nexus · Curated by Lauren Lowenstein, The Biotoxin Lady

Key Biomarkers

Symptom Clusters