Thrombotic Microangiopathy and Increased Nitrosative and Oxidative Stress in an Animal Model of Induced Sepsis 23rd European Congress of Pathology Helsinki, 2011. R Granados, L El Bouayadi, N Nin, A Ferruelo, C Sánchez, Y Rojas, P Cardinal, A Esteban, M de Paula, JA Lorente
Thrombotic Microangiopathy and Increased Nitrosative and Oxidative Stress in an Animal Model of Induced Sepsis23rd European Congress of PathologyHelsinki, 2011
R Granados, L El Bouayadi, N Nin, A Ferruelo, C Sánchez, Y Rojas, P Cardinal, A Esteban, M de Paula, JA Lorente
Hospital Universitario de Getafe, Madrid
1.-To study the morphology of the lesions associated to sepsis.
2.-To measure the genetic expresion of some mediators of oxidative and nitrosative stress.
- Inducible Nitric Oxyde Synthase (iNOS)
- Tumor Necrosis factor (TNF)
- Nitrotyrosine (NT)
- Interleukine 6 (IL-6)
3.-To quantify the degree of protein nitration and oxydation.
Global glomerular damage
Segmental glomerular damage
Acute Tubular Necrosis
PAS positive granules in proximal tubules
Absence of vascular damage
NITRATION AND OXIDATION
TNF, IL-6 and NGAL were significantly elevated in septic animals
TNF: 5109,9/0,13 ng/ug protein
IL6: 1296/0,27 ng/ug protein
NGAL: 1121,15/172,98 ng/ml
Significant elevation of NT protein and iNOS was seen in the renal cortex of septic animals.
NT: control: 3688, sepsis: 8900
iNOS: control:7628, sepsis: 10776
Increased gene expression of TNF, IL-6 and iNOS, was seen in renal cortex of septic animals
Centro Nacional de Biotecnología, CSIC, Madrid, Spain. Juan Ortín, Lorena Ver