There is growing evidence that myocardial dysfunction in 'septic shock is induced by mediators of the systemic inflammatory respopse syndrome, in particular by cytokines such as tissue necrosis factor-a (TNF-a) and interleukin-1 (IL-1). TNF-a produces an immediate negative inotropic effect by alteration in intracellular calcium homeostasis. Longer term effects of TNF-a and IL-1 may involve increased expression of NO synthase and decreased responsiveness of p-adrenergic stimulation. Most recently, strategies have been formulated to try and inhibit or attenuate toxic effects of TNF-a and IL-1; this has included the use of anti-TNF-a antibodies, soluble receptors for TNF-a, and recombinant IL-1 receptor antagonists.