Effects of long-term intravenous and intragastric L-arginine intervention on jejunal motility and visceral nitric oxide production in the hyperdynamic compensated endotoxaemic pig.

Alterations in L-arginine availability and nitric oxide (NO) synthesis in the intestinal muscularis may contribute to disturbed small intestinal motility that is observed during endotoxaemia. The aim of this study was to evaluate the effect of L-arginine infusion on visceral NO production and jejunal motility in hyperdynamic compensated endotoxaemic pigs. Fasted and saline-resuscitated pigs were intravenously infused for 24 h with endotoxin (lipopolysaccharide, 50 ng kg(-1) min(-1)) or saline (n = 6). Endotoxaemic pigs received either intravenous L-arginine (n = 6, 5.3 micromol kg(-1) min(-1)) or L-alanine (isocaloric, n = 6). After 24 h, intravenous L-arginine or L-alanine infusion was continued intragastrically for 32-h in an enteral meal. During (0-24 h) and 1 day postendotoxaemia (48-56 h), jejunal motility was recorded by manometry and analysed for migrating motor complex (MMC) characteristics. Visceral NO production was measured at 24 and 48 h by 15N2-arginine-to-15N-citrulline conversion. Visceral NO production was increased during endotoxaemia and was higher in L-arginine than in L-alanine-treated pigs. One day postendotoxaemia, visceral NO synthesis was still increased in L-arginine but not in L-alanine-treated animals. Endotoxaemia shortened the MMC cycle duration and accelerated the MMC propagation velocity. Both were restored by L-arginine. Similar motility disturbances were observed one day postendotoxaemia and were also compensated by L-arginine infusion.