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Myocardial dysfunction in septic shock: Part II. Role of cytokines and nitric oxide.

The question of whether humans exhibit true myocardial depression (ie, independent of loading conditions) in sepsis and septic shock had existed since the early studies of experimental endotoxic shock in animals in the 1950s and early 1960s.1,2 Using a novel application of nuclear imaging technology, Parker et al,3 in the early 1980s, definitively showed the existence of human septic myocardial depression (decreased biventricular ejection fraction despite increased cardiac output). The cause of such depression remained in doubt, however. Two major theories regarding the nature of septic myocardial depression in humans and animals existed. The first theory suggested that sepsis was associated with globally decreased myocardial perfusion resulting in ischemic injury to the septic heart. This theory had been supported by many investigators based, in part, on evidence of global myocardial hypoperfusion in canine models of endotoxic shock.4-8 As it became apparent that endotoxic shock is not an appropriate model through which to study septic myocardial dysfunction, another theory rose to prominence. The origins of the second major theory regarding the nature of myocardial depression in septic shock are found in Wigger’s classic 1947 report9 proposing the presence of a myocardial depressant factor in experimental hemorrhagic shock. By the 1960s, other investigators had suggested that a similar circulating depressant substance was responsible for septic myocardial depression in humans with septic shock.10,11