It is suggested that pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), act directly or indirectly to depress cardiac function resulting in endotoxemia-induced myocardial dysfunction [4,5], and inhibition of the production of inflammatory mediators in the heart attenuates lipopolysaccharide (LPS)-induced myocardial dysfunction [6]. Here, TNF is linked to serum lipopolysaccharide activity.