[Seventh Jesús Culebras Lecture. Systemic inflammatory response and multi organic dysfunction/failure following aggression: metabolic implications].

Following any aggression, the body starts an infl ammatory 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 infl ammatory cells is originated, with liberation of immature cells and activation of monocytes and macrophages, which liberate very powerful pro infl ammatory mediators that induce a state of generalized systemic infl ammation. Many processes may originate this infl ammatory 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 infl ammation, 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