Effect of Previous High Glutamine Infusion on Inflammatory Mediators and Mortality in an Acute Pancreatitis Model

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.

The Beneficial Effects of Lipoic Acid Versus Coenzyme Q10 on Arginine-Induced Acute Pancreatitis in Albino Rats: Histological and Immunohistochemical study

“…An increase in the expression of Hsp70 is associated with an improvement in survival, less tissue damage, and a decreased inflammatory response [38] . In the case of AP induced by sodium taurocholate in rats, the administration of glutamine favors the expression of HSP70, conferring protection from the organic damage induced by the illness [23] . HSP70 regulates the inflammation response through various mechanisms, one of which is the inhibition of the secretion of HMGB1 [39] .…”

“…NF-κB p65 is a rabbit polyclonal antibody with a cytoplasmic reaction. It was used for the detection of tissue inflammation [23] . Pancreatic tissue samples were fixed in neutral buffered formalin, embedded in paraffin, sectioned, and mounted on slides.…”

A Comparison of Oral and Intravenous Glutamine Therapy Effects On Mucositis Development in Acute Leukemic Patients After High Dose Chemotherapy Supplementation

“…In a study, Ricardo Garib et al evaluated the inflammatory and survival responses after parenteral glutamine infusion in experimental acute pancreatitis. They suggest that a high dose of parenteral glutamine protects against stress-induced organ damage by improving cytokine profiles [20].…”

Emodin in Severe Acute Pancreatitis Treatment

“…The inflammatory mediators associated with severe acute pancreatitis include interleukin (IL), tumor necrosis factor (TNF), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and platelet activating factor, which are correlated and exert mutual influence [21]. IL-1 is produced in the early stage of inflammation and plays an important role in the early phase of se- pro-inflammatory mediators [22].…”