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The understanding of nitric oxide signaling in sepsis-induced cardiac dysfunction has evolved from a simple uniform depressant model to a complex, domain-specific regulatory mechanism.
ur initial understanding that the inhibition of inducible nitric oxide synthase (iNOS or NOS2) dependent NO production in cardiac myocytes would restore contractile function and improve outcome in septic shock failed. 1 This was, in part, because of our then lack of understanding of the complexity of NO signaling in the cardiovascular system in health and disease. The initial paradigm that NO acts as a diffusible molecule to depress cardiovascular function uniformly and diffusely has been replaced by a more sophisticated yet incomplete model of NO signaling. It calls for NO to act in very defined signaling domains, through distinct signal transduction mechanism, sub-serving focused physiologic functions. It is now well established that NO and NO-related species are significant modulators of cardiac muscle excitation-contraction coupling and that these species affect a number of molecules and channels that coordinate this process.
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Dan E. Berkowitz (2007) studied this question.
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