PMN superoxide radical production following a metabolic-endocrine simulation of trauma.
Serious infections following major trauma remain inexplicably high. Metabolic and endocrine changes after injury have been suggested as being responsible for many of the documented defects in the polymorphonucleocyte (PMN). The in vitro bactericidal activity of normal human PMNs has been examined in this laboratory by assaying the activity of the PMN membrane bound enzyme NADPH oxidase and hence O2- production of the PMN in a metabolic/endocrine milieu designed to simulate moderately severe trauma. This was accomplished by incubating the PMN with physiological and trauma serum concentrations of insulin, glucose, cortisol, epinephrine, and glucagon. The results indicate that the O2- production of the PMN is significantly enhanced in this environment. It would appear that exogenous glucose alone was responsible for this enhanced O2- production.
D000328:Adult; D004837:Epinephrine / Q000502:physiology; D005609:Free Radicals; D005934:Glucagon / Q000502:physiology; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000502:physiology; D066298:In Vitro Techniques; D007328:Insulin / Q000502:physiology; D008297:Male; D009247:NADH, NADPH Oxidoreductases / Q000032:analysis; D019255:NADPH Oxidases; D009504:Neutrophils / Q000378:metabolism*; D010100:Oxygen / Q000096:biosynthesis; D013481:Superoxides / Q000378:metabolism*; D014947:Wounds and Injuries / Q000201:enzymology / Q000378:metabolism* / Q000503:physiopathology
D005609:Free Radicals; D007328:Insulin; D013481:Superoxides; D005934:Glucagon; D009247:NADH, NADPH Oxidoreductases; D019255:NADPH Oxidases; D005947:Glucose; D010100:Oxygen; D006854:Hydrocortisone; D004837:Epinephrine