In vitro effect of canine hyperimmune sera on TNFa activity

Abstract

[Introduction]: Septic shock in dogs is caused by cardiovascular and vasomotor failure associated with an uncontrolled intrinsic release of inflammatory mediators [1–5]. The syndrome is characterized by cardiovascular dysfunction, vascular permeability alterations, pulmonary oedema and tissue hypoxia resulting from microthrombi which may culminate in disseminated intravascular coagulation and catastrophic multiple organ failure [6,7]. Systemic bacterial infection, particularly by Gram-negative enterobacteria, haemorrhagic trauma, gastric dilation/volvulus and pancreatitis are the major underlying causes leading tosepsis [8,9]. Because of haemodynamic instability and associated hypovolemia, fluid replacement therapy is generally applied to restore effective circulating volume. The use of fresh frozen plasma has been recommended in cases of coagulopathies as it has been recognized to assist restoration of haemodynamic stability [1,5,10,11]. There is increasing evidence that the drivers of the haemodynamic instability are inflammatory mediators (particularly TNFa) activated primarily by bacterial endotoxin [3,4,12,13].