Metabolic and Clinical Effects of the Supplementation of a Functional Mixture of Amino Acids in Cerebral Hemorrhage

Oral supplementation of a specific mixture of essential and non-essential amino acids has been shown to modulate hypercatabolism in patients with chronic heart failure, leading to improved clinical outcome. The aim of this study was to test whether such effects could be replicated in an acute clinical model of hypercatabolism. After approval by the Ethics Committee, patients with acute brain hemorrhage admitted to the Neurosurgical ICU were randomly assigned to receive enterally for 14 days 20% of their estimated nitrogen requirements as a standard protein supplement (control group; n = 9) or as a functional amino acid mixture (Aminotrofic(A (R)), Errekappa Euroterapici; study group; n = 10). Metabolic and clinical outcome measures were monitored. In the study group, insulin sensitivity and total lymphocyte count appeared to improve when compared with control patients. Less positive blood cultures were found in the study group against control patients (4 vs. 7, respectively; P = 0.05). Also, mortality in the study group was reduced than in control patients (60 vs. 77%; P = n.s.). Supplementation with specific amino acids in critically ill patients may modulate metabolic response and improve clinical outcome

Stress-induced facilitation of host response to bacterial challenge in F344 rats is dependent on extracellular heat shock protein 72 and independent of alpha beta T cells

Activation of the in vivo stress response can facilitate antibacterial host defenses. One possible mechanism for this effect is stress-induced release of heat shock protein 72 (Hsp72) into the extracellular environment. Hsp72 is a ubiquitous cellular protein that is up-regulated in response to cellular stress, and modulates various aspects of immune function including macrophage inflammatory/bactericidal responses and T-cell function when found in the extracellular environment. The current study tested the hypothesis that in vivo extracellular Hsp72 (eHsp72) at the site of inflammation contributes to stress-induced restricted development of bacteria, and facilitated recovery from bacteria-induced inflammation, and that this effect is independent of alpha beta (αβ) T cells. Male F344 rats were exposed to either inescapable electrical tail-shocks or no stress, and subcutaneously injected with Escherichia coli (ATCC 15746). The role of eHsp72 was investigated by Hsp72-immunoneutralization at the inflammatory site. The potential contribution of T cells was examined by testing male athymic (rnu/rnu) nude rats lacking mature αβ T cells and heterozygous thymic intact control (rnu/) rats. The results were that stressor exposure increased plasma concentrations of eHsp72 and facilitated recovery from bacterial inflammation. Immunoneutralization of eHsp72 at the inflammatory site attenuated this effect. Stressor exposure impacted bacterial inflammation and eHsp72 equally in both athymic and intact control rats. These results support the hypothesis that eHsp72 at the site of inflammation, and not αβ T cells, contributes to the effect of stressor exposure on subcutaneous bacterial inflammation. © 2012 Informa Healthcare USA, Inc