RESUMEN
The inflammatory response syndrome in shock-like states might frequently be accompained by an oxidative cell/tissue demage in one or more organ-systems in the body. The inflammatory response related hyperactivation of neutrophils can contribute to oxidative cell/tissue damage. Studies discussed in this review examined the role of cell sgnaling pathways in the hyperactivation of neutrophils in an early stage of burn injury shock. The studies were carried out in peripheral blood neutrophils isolated from rats with a 25 per cent body surface area scald burn. Neutrophil cell signaling responses were evaluated by measuring cytosolic [Ca2+] and protein kinase C activity, and were correlated with neutrophil superoxide production. The cytosolic [Ca2+] and protein kinase C responses were highly upregulated along with enhanced superoxide production in the early phase of burn injury. The treatment of burn-injured rats with the calcium antagonist diltiazem abrogated enhanced Ca2+ and protein kinase C signaling and superoxide generation. The signaling upregulation in neutrophils could result from potentiation of actions of burn-injury induced chemotactic mediators on the leukocytes. The neutrophil signaling upregulation leading to increased superoxide generation could thus be responsible for the oxidative cell/tissue damage. The organ-system dysfunction/failure accompanying burn shock may be initiated with the oxidative cell/tissue damage.