Background-There is evidence that endogenous nitrate synthesis is notably increased in patients with infective gastroenteritis.
Aims-To determine whether this is due to nitric oxide (NO) production via the L-arginine/NO pathway.
Methods-Seven male patients with community acquired bacterial gastroenteritis and 15 healthy male volunteers participated in this study, All patients had stool culture positive infective gastroenteritis. A bolus of 200 mg L-[N-15](2)-arginine was administered intravenously after an overnight fast. Urine was collected for the next 36 hours. Urinary [N-15:N-14]nitrate ratio was assessed by dry combustion in an isotope ratio mass spectrometer.
Results-Mean 36 hour total urinary nitrate excretion in the gastroenteritis group was 5157 (577) mu mol compared with 2594 (234) mu mol in the control group (p<0.001). Thirty six hour urinary [N-15]nitrate excretion was considerably higher in the gastroenteritis group compared with the control group (13782 (1665) versus 1698 (98) eta mol; p<0.001). These values represent 1.129 (0.139)% and 0.138 (0.007)% of [N-15]nitrogen administered (p<0.001), respectively. Corrected 36 hour urinary [N-15]nitrate excretion for urinary creatinine was also significantly higher in the patient compared with the control group (1934 (221) versus 303 (35) eta mol/mmol; p<0.001).
Conclusion-Results show notably enhanced nitrate synthesis due to increased activity of the L-arginine/NO pathway in patients with infective gastroenteritis.
- endothelium derived relaxing factor
- inflammatory bowel-disease
- colon epithelial-cells
- plasma nitrate concentration
- active ulcerative-colitis
- challenge in-vivo
- synthase activity
- bacterial translocation
- endotoxin challenge