Effects of pharmaconutrients on cellular dysfunction and the microcirculation in critical illness.

Journal Article (Journal Article;Review)

PURPOSE OF REVIEW: A growing body of data has revealed that specific nutrient deficiencies contribute to microvascular and cellular dysfunction following critical illness. Further, targeted administration of these 'pharmaconutrients' may reverse or improve this dysfunction and improve clinical outcome. RECENT FINDINGS: Specific nutrient therapy with glutamine protects cellular metabolism and vascular function via induction of heat shock proteins, which are key proteins found to be deficient following acute illness. Arginine becomes rapidly deficient following trauma and surgery. This leads to significant immunosuppression, which when treated by arginine administration significantly reduces postoperative infection. Omega-3 fatty acids attenuate the inflammatory response and provide for resolution of ongoing inflammatory injury via production of resolvins/protectins. Antioxidants (vitamin C and selenium) and trace elements (zinc) become rapidly depleted in critical illness and replacement appears vital to ensure optimal cellular and microvascular function. Data on targeted metabolic (mitochondrial) therapies (i.e. co-enzyme Q10) show promise to improve myocardial function following cardiac surgery. SUMMARY: These specific nutrients have newly discovered vital mechanistic roles in the optimization of cellular and microcirculatory function in critical illness and injury. A growing body of literature is demonstrating that correction of key nutrient deficiencies via therapeutic administration of these pharmaconutrients can improve clinical outcome in critically ill patients.

Full Text

Duke Authors

Cited Authors

  • Weitzel, L-RB; Mayles, WJ; Sandoval, PA; Wischmeyer, PE

Published Date

  • April 2009

Published In

Volume / Issue

  • 22 / 2

Start / End Page

  • 177 - 183

PubMed ID

  • 19307892

Electronic International Standard Serial Number (EISSN)

  • 1473-6500

Digital Object Identifier (DOI)

  • 10.1097/ACO.0b013e328328d32f


  • eng

Conference Location

  • United States