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Intensive Care Medicine pp 186–203Cite as

Regulatory Role of Nitric Oxide in the Heart of the Critically Ill Patient

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Abstract

More than two decades ago, Furchgott and Zawadzki [1] discovered that intact endothelium was necessary for acetylcholine-induced vasorelaxation. A substance derived from this endothelium, the so-called ‘endothelium-derived relaxing factor’ (EDRF), was born. It took until 1988 for this to be identified as nitric oxide (NO) [2]. In addition to its release in the coronary circulation, NO also reduced contractility in cultured cardiomyocytes [3, 4] and was shown to mediate, at least in part, the septic cardiodepression induced by the ‘myocardial depressant substance’, identified as the combination of tumor necrosis factor (TNF)-a and interleukin (IL)-1 [5]. Since then, this highly diffusable gas has been found to be nearly ubiquitous in the organism in a large variety of cellular types and organs, and implicated in almost all cardiovascular, neuronal, and immune processes.

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  1. P. B. Massion
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  2. J. L. Balligand
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Editors and Affiliations

  1. Department of Intensive Care, Erasme Hospital, Free University of Brussels, Route de Lennik 808, B-1070, Brussels, Belgium

    Jean-Louis Vincent MD, PhD, FCCM, FCCP (Head) (Head)

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Massion, P.B., Balligand, J.L. (2002). Regulatory Role of Nitric Oxide in the Heart of the Critically Ill Patient. In: Vincent, JL. (eds) Intensive Care Medicine. Springer, New York, NY. https://doi.org/10.1007/978-1-4757-5551-0_17

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