INVESTIGADORES
PODEROSO Juan Jose
congresos y reuniones científicas
Título:
Nitric Oxide, neutrophils and sepsis.
Autor/es:
CARRERAS MC; CATZ SD; PARGAMENT GA; DEL BOSCO CG; PODEROSO JJ
Lugar:
Basilea, Suiza
Reunión:
Congreso; Second International Symposium on Endothelium-derived Vasoactive factors; 1992
Resumen:
Sepsis (S) involves hemodynamical and vascular endothelial changes mediated by cytokines like tumor necrosis factor (TNF); vasodilation could reflect effects of TNF on endothelial nitric oxide (NO) production. Neutrophils (PMN) release NO and are also activated by TNF; the aim of this work was to determine NO and oxidative responses by PMN in S. We studied 17 patients with moderate to severe S and 20 healthy subjects (C); PMN were isolated by Ficoll-Hypaque sedimentation. The NO was measured in supernatants by Griess reaction at variousperiods with L-arginine or N-monomethyl L-arginine (NMMA) and superoxide anion (O2-) by standard methods with different stimulators. The results shoed a decreased NO production in pmoles NO2-/106 PMN at 2 min C: 290±28 vs S: 165±27, p<0.005; at 30 min, C: 449±39 vs S:280±33, p<0.005. Preincubation with TNF (1,000 U7ML) did not increase NO production by PMN in S and, furthermore, it diminished this variable in controls, C: 311±20, C+TNF: 248±10, p<0.01, C+ NMMA: 229±22, p<0.01. In S, PMN had a decreased oxidative burst response to TNF priming, in nmol O2-/106 PMN/min, C+TNF: 1.1±0.2 vs S+TNF: 0.6±0.1, p<0.025. We believe that, in contrast to the endothelium, NO production by PMN is diminished up to NMMA levels in some stages of S with a concomitant decrease of O2- release; this fact could be mediated by TNF and it suggests an impairment of different PMN functions during sepsis.