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Etiology of Decreased Gastric Nitric Oxide in the Critically Ill
  1. Michel A. Boivin,
  2. Christopher A. Fiack,
  3. John C. Kennedy,
  4. Gary K. Iwamoto
  1. From the Department of Medicine (M.A.B., J.C.K., G.K.I.), University of New Mexico, Albuquerque, NM; The Pulmonary Center (C.A.F.), Boston University School of Medicine, Boston, MA.
  1. Supported by the National Institutes of Health, National Center for Research Resources, General Clinical Research Center, grant 5MO1 RR00997. Dr. Boivin was also funded by dedicated health research funds of the University of New Mexico.
  2. Presented in part at the Western Section of the American Federation for Medical Research annual meeting in Carmel, CA, January 2003.
  3. Address correspondence to: Dr. Michel A. Boivin, UNM School of Medicine, 1 UNM, MSC 10-5550, Albuquerque, NM 87131; e-mail: mboivin{at}


Background Nitric oxide (NO) is present in the gas phase of the normal human stomach at a high concentration (1-10 ppm). The majority of this NO is produced from the reduction of dietary nitrate to nitrite and finally NO. Generation of this nonenzymatically produced gastric NO occurs only in an acidic environment. We examined NO concentrations in critically ill subjects and the mechanism for the observed perturbations.

Methods Seven critically ill, intubated intensive care unit (ICU) patients (mean APACHE II score 16) and seven control patients were studied. Gastric NO concentrations were measured with a Sievers NO analyzer (GE, Boulder, CO). Nitrate and nitrite concentrations were determined by a modified Griess assay. Bacterial counts were determined by optical density at 600 nm.

Results Gastric NO concentration was significantly lower in the critically ill group (102.7 ppb) compared with the control group (953.2 ppb), although this difference was abolished by treating the control group with omeprazole (54 ppb). Gastric nitrate and nitrite concentrations were similar in the control and ICU groups, suggesting that substrate deficiency was not a cause of the low intragastric NO. Gastric pH was significantly lower in the control subjects (3.0) compared with the ICU patients (6.3) and the control subjects after receiving omeprazole (6.5). ICU patients had a trend toward higher gastric bacterial load.

Conclusion In critically ill patients, markedly decreased NO concentrations are found in the gas of the stomach owing to a failure of gastric acidification.

Key words
  • nitric oxide
  • bacteria
  • critical care

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