Nitric oxide synthesis in patients with infective gastroenteritis

Abstract

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-[(15)N](2)-arginine was administered intravenously after an overnight fast. Urine was collected for the next 36 hours. Urinary [(15)N:(14)N]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) micromol compared with 2594 (234) micromol in the control group (p<0.001). Thirty six hour urinary [(15)N]nitrate excretion was considerably higher in the gastroenteritis group compared with the control group (13782 (1665) versus 1698 (98) etamol; p<0.001). These values represent 1.129 (0.139)% and 0.138 (0.007)% of [(15)N]nitrogen administered (p<0.001), respectively. Corrected 36 hour urinary [(15)N]nitrate excretion for urinary creatinine was also significantly higher in the patient compared with the control group (1934 (221) versus 303 (35) etamol/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.

Figure 1

Cumulative urinary excretion of [¹⁵N]nitrate after intravenous administration of L-[¹⁵N]₂-guanidino arginine in patients and controls. Values are mean (SEM) for seven patients and 15 healthy volunteers. *Significant difference between healthy volunteers and patients (p<0.001).