Resumen

GARCIA DE LORENZO Y MATEOS, Abelardo. Seventh Jesús Culebras Lecture. Systemic inflammatory response and multi organic dysfunction/failure following aggression: metabolic implications. Nutr. Hosp. [online]. 2017, vol.34, n.1, pp.244-250. ISSN 1699-5198.  https://dx.doi.org/10.20960/nh.1001.

Following any aggression, the body starts an inflammatory response, mediated by humoral and cellular factors, intended to limit the process and eventually to heal. In some cases, either due to the intensity or the duration of the aggression or due to an inadequate response of the host, secondary to genetic polymorphisms, malnutrition or other causes, a state of hyper activation of inflammatory cells is originated, with liberation of immature cells and activation of monocytes and macrophages, which liberate very powerful pro inflammatory mediators that induce a state of generalized systemic inflammation. Many processes may originate this inflammatory response, (sepsis, trauma, burns, pancreatitis, etc.) with activation of leukocyte, endothelial, coagulation and neuroendocrine response systems, generating a complex of mediators (cytokines, adhesion molecules, growth factors, etc.). Clinically, the response is characterized by inflammation, anorexia, stillness, increase of vascular permeability, factors that originate edema and vasodilatation, which is followed by hypotension, tachycardia and increased cardiac output. On the other hand, the metabolic response to stress is part of the mechanism of adaptation, generated by the organism in order to survive the acute disease by means of increasing energetic substrates to vital tissues. As a result of this complex metabolic response, the control of substrate utilization is only partially regulated because, being impaired the mechanisms of energy supply, the organism seeks alternative substrates.

Palabras clave : Systemic proinflammatory response; Compensatory anti-inflammatory response syndrome; Molecular adsorbents recirculation system; Persistent systematic inflammatory response syndrome; Multiorganic failure; Injury; Metabolism.

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