Abstract
Parenteral glutamine supplementation in acute inflammatory conditions is controversial. We evaluated the inflammatory and survival responses after parenteral glutamine infusion in sodium taurocholate-induced acute pancreatitis (AP) model. Lewis rats received 1 g/kg parenteral glutamine (n = 42), saline (n = 44), or no treatment (n = 45) for 48 h before AP induction. Blood, lung, and liver samples were collected 2, 12, and 24 h after AP to measure serum cytokines levels and tissue heat shock protein (HSP) expression. From each group, 20 animals were not sacrificed after AP for a 7-day mortality study. Serum cytokine levels did not differ among groups at any time point, but the intragroup analysis over time showed higher interferon-γ only in the nontreatment and saline groups at 2 h (versus 12 and 24 h; both p ≤ 0.05). The glutamine group exhibited greater lung and liver HSP90 expression than did the nontreatment group at 2 and 12 h, respectively; greater liver HSP90 and HSP70 expression than did the saline group at 12 h; and smaller lung HSP70 and liver HSP90 expression than did the nontreatment group at 24 h (all p ≤ 0.019). The 7-day mortality rate did not differ among groups. In experimental AP, pretreatment with parenteral glutamine was safe and improved early inflammatory mediator profiles without affecting mortality.
Highlights
Glutamine can become essential during hypercatabolic stress and under critical conditions, such as severe trauma, sepsis, inflammatory diseases, and burns [1]
The present study aimed to evaluate the impact of previous parenteral glutamine infusion on inflammatory mediator levels and mortality in acute critically ill conditions, using experimental acute pancreatitis (AP) as a systemic inflammation-reproducing model
Our study aimed to contribute to the understanding of potential inflammatory mechanisms that may impact the riskbenefit balance of parenteral glutamine infusion in critical care
Summary
Glutamine can become essential during hypercatabolic stress and under critical conditions, such as severe trauma, sepsis, inflammatory diseases, and burns [1]. Glutamine is a fuel source for lymphocytes and enterocytes, a substrate for glutathione and heat shock protein (HSP) synthesis, and a potential inhibitory agent for inflammatory cytokine release [2, 3]. These biological properties could contribute to improving gut barrier and lymphocyte function and to attenuate inflammatory responses [4]. Glutamine supplementation has been suggested to properly support increased cell proliferation rates, gut barrier protection, and inflammatory dysfunction attenuation [5, 6]. Unexpected harmful effects of parenteral glutamine supply, mainly in patients with multiple organ failure, have been reported recently [7,8,9]
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