Objective: To determine whether parenteral feeding (IV-TPN) influences the local and systemic response to an intestinal insult.
Summary Background Data: Parenteral feeding increases ICAM-1 expression and attracts neutrophils (PMNs) to the intestine compared with enterally fed animals. Because the gut is a priming bed for PMNs, the authors hypothesized that IV-TPN may affect organ injury after gut ischemia-reperfusion (I/R).
Methods: Mice were randomized to chow, IV-TPN, intragastric TPN, or complex enteral diet for 5 days' feeding. In experiment 1, 162 mice underwent 15 or 30 minutes of gut I/R, and death was recorded at 72 hours. In experiment 2, 43 mice underwent 15 minutes of gut ischemia and permeability was measured by 125I-labeled albumin at 3 hours after reperfusion. Lung PMN accumulation was measured by myeloperoxidase assay. In experiment 3, albumin leak was tested in the complex enteral diet group (n = 5) and the intragastric TPN group (n = 5) after 30 minutes of gut ischemia and 1 hour of reperfusion.
Results: In experiment 1, enteral feeding significantly reduced the death rate compared with IV-TPN after 15 minutes of I/R. After 30 minutes of gut ischemia, the IV-TPN and intragastric TPN groups showed a higher death rate than the chow and enteral diet groups. In experiment 2, IV-TPN significantly increased pulmonary and hepatic 125I albumin leak compared with enteral feeding without increasing pulmonary myeloperoxidase levels. In experiment 3, there were no differences in 125I albumin leak between the complex enteral diet and intragastric TPN groups.
Conclusion: Enteral feeding reduced the death rate and organ permeability after 15 minutes of ischemia. However, prolonged ischemia (30 minutes) eliminated any benefits of intragastric TPN on survival.
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http://dx.doi.org/10.1097/00000658-200105000-00010 | DOI Listing |
J Surg Res
February 2018
Department of Surgery, National Defense Medical College, Saitama, Japan.
Background: Enteral nutrition (EN) is the gold standard of nutritional therapy for critically ill or severely injured patients, because EN promotes gut and hepatic immunity, thereby preventing infectious complications as compared with parenteral nutrition. However, there are many EN formulas with different protein and fat contents. Their effects on gut-associated lymphoid tissue remain unclear.
View Article and Find Full Text PDFJ Surg Res
September 2008
Division of Traumatology, National Defense Medical College Research Institute, Saitama, Japan.
Background: Although early enteral nutrition after insult has many advantages, effects of early nutritional manipulation on outcome after gut ischemia-reperfusion (I/R) remain unclear. We hypothesize that early enteral nutrition would improve survival after severe gut I/R by reducing organ injury and leukocyte activation.
Materials And Methods: Mice were randomized to chow, intravenous (IV)-total parenteral nutrition (TPN), intragastric (IG)-TPN, or complex enteral diet (CED) for feeding after I/R.
Ann Surg
April 2007
Department of Surgery I, Chiba University, Chiba, Japan.
Objective: To clarify the influence of nutritional route on hepatic immunity in a murine model.
Summary Background Data: Parenteral nutrition is disadvantageous for preventing infectious complications in critically ill and/or severely injured patients as compared with enteral nutrition. To date, lack of enteral nutrition has been demonstrated to impair mucosal immunity, gut barrier function, and the peritoneal defense system.
Shock
March 2007
Department of Surgery, National Defense Medical College Research Institute, Saitama, Japan.
The mitogen-activated protein kinase (MAPK) family (extracellular-regulated kinase [ERK], p38, etc.) of signal transduction proteins includes important intracellular mediators of inflammation, playing critical roles in host defense. Phosphorylations of ERK and p38 are responsible for cell proliferation, cell differentiation, and cell death.
View Article and Find Full Text PDFShock
October 2005
Department of Surgery I, National Defense Medical College, Saitama, Japan.
Morbidity of intra-abdominal abscess is increased when severely injured patients are fed parenterally. Lack of enteral nutrition appears to impair peritoneal cavity host defense. Because the transcription factor nuclear factor kappaB (NFkappaB) regulates various genes involved in inflammatory responses and its activation is important for host defense, we hypothesized that enteral nutrition would preserve appropriate NFkappaB activation in peritoneal resident cells (PRCs), the first defense line against peritoneal contamination.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!