Duodenal nutrient exposure contributes to enhancing gastric accommodation.

BACKGROUND: The gastric accommodation reflex consists of a relaxation which creates a reservoir for the ingested food before emptying to the duodenum occurs. The mechanisms that control gastric accommodation are not fully understood. This study aims to use intragastric pressure (IGP) measurement and pyloric balloon obstruction to determine the contribution of duodenal nutrient exposure to gastric accommodation and meal-induced satiation. METHODS: Two conditions were tested in 11 healthy subjects (28.3 ± 3.2 years; 23.6 ± 0.7 kg/m2 ; four females). IGP was measured during an intragastric nutrient drink (ND) infusion at a constant rate (60 mL/min) in the presence of a deflated (control) or inflated (pyloric obstruction) balloon placed into the pylorus. During the study, subjects filled out Likert scales for satiation scores and visual analogue scale for 9 epigastric symptoms (hunger, expected amount to eat, satiation, bloating, fullness, nausea, belching, gastric cramps, and pain) before and during ND infusion until maximal satiation. KEY RESULTS: During pyloric obstruction, the IGP drop and the area above the IGP curve (AAC) were significantly smaller compared with the control condition (6.7 ± 1.0 mm Hg vs3.6 ± 0.8 mm Hg, P = .03 and 69.7 ± 13.5 mm Hg × min vs 20.1 ± 9.0 mm Hg × min, P = .001, respectively). Pyloric obstruction decreased nutrient tolerance compared with the control condition (787.9 ± 73.1 mL vs 970.9 ± 79.2 mL, respectively, P < .05). Pyloric obstruction increased symptoms of bloating (1.3 ± 0.4 vs 2.6 ± 0.6; P = .04), fullness (2.3 ± 0.5 vs 3.6 ± 0.3; P = .03), and nausea (0.4 ± 0.2 vs 1.3 ± 0.4; P = .04) compared to control. CONCLUSION & INFERENCES: Duodenal nutrient exposure contributes to enhancing gastric accommodation. Preventing the passage of nutrients from the stomach to the duodenum inhibits gastric accommodation and increases meal-induced satiation, bloating, nausea, and fullness.

Effect of pancreatic polypeptide on gastric accommodation and gastric emptying in conscious rats.

Pancreatic polypeptide (PP) is an anorexigenic hormone released from pancreatic F cells upon food intake. We aimed to determine the effect of PP on gastric accommodation and gastric emptying in conscious Wistar HAN rats to investigate whether effects on motor function could contribute to its anorexigenic effects. Intragastric pressure (IGP) was measured through a chronically implanted gastric fistula during the infusion of a nutrient meal (Nutridrink; 0.5 ml/min). Rats were treated with PP (0, 33 and 100 pmol·kg(-1)·min(-1)) in combination with N(G)-nitro-L-arginine methyl ester (L-NAME; 180 mg·kg(-1)·h(-1)), atropine (3 mg·kg(-1)·h(-1)), or vehicle. Furthermore, the effect of PP was tested after subdiaphragmal vagotomy of the stomach. Gastric emptying of a noncaloric and a caloric meal after treatment with 100 pmol·kg(-1)·min(-1) PP or vehicle was compared using X-rays. PP significantly increased IGP during nutrient infusion compared with vehicle (P < 0.01). L-NAME and atropine significantly increased IGP during nutrient infusion compared with vehicle treatment (P < 0.005 and 0.01, respectively). The effect of PP on IGP during nutrient infusion was abolished in the presence of L-NAME and in the presence of atropine. In vagotomized rats, PP increased IGP compared with intact controls (P < 0.05). PP significantly delayed gastric emptying of both a noncaloric (P < 0.05) and a caloric (P < 0.005) meal. PP inhibits gastric accommodation and delays gastric emptying, probably through inhibition of nitric oxide release. These results indicate that, besides the well-known centrally mediated effects, PP might decrease food intake through peripheral mechanisms.

Psychological stress and corticotropin-releasing hormone increase intestinal permeability in humans by a mast cell-dependent mechanism.

OBJECTIVE: Intestinal permeability and psychological stress have been implicated in the pathophysiology of IBD and IBS. Studies in animals suggest that stress increases permeability via corticotropin-releasing hormone (CRH)-mediated mast cell activation. Our aim was to investigate the effect of stress on intestinal permeability in humans and its underlying mechanisms. DESIGN: Small intestinal permeability was quantified by a 2 h lactulose-mannitol urinary excretion test. In a first study, 23 healthy volunteers were subjected to four different conditions: control; indomethacin; public speech and anticipation of electroshocks. In a second study, five test conditions were investigated in 13 volunteers: control; after pretreatment with disodium cromoglycate (DSCG); administration of CRH; DSCG+CRH and DSCG+public speech. RESULTS: Indomethacin, as a positive comparator (0.071±0.040 vs 0.030±0.022; p<0.0001), and public speech (0.059±0.040; p<0.01), but not the shock protocol increased intestinal permeability. Similarly, salivary cortisol was only increased after public speech. Subgroup analysis demonstrated that the effect of public speech on permeability was only present in subjects with a significant elevation of cortisol. CRH increased the lactulose-mannitol ratio (0.042±0.021 vs 0.028±0.009; p=0.02), which was inhibited by the mast cell stabiliser DSCG. Finally, intestinal permeability was unaltered by public speech with DSCG pretreatment. CONCLUSIONS: Acute psychological stress increases small intestinal permeability in humans. Peripheral CRH reproduces the effect of stress and DSCG blocks the effect of both stress and CRH, suggesting the involvement of mast cells. These findings provide new insight into the complex interplay between the central nervous system and GI function in man.

Experimental comparison of abdominal wall repair using different methods of enhancement by small intestinal submucosa graft.

INTRODUCTION AND HYPOTHESIS: To assess the biomechanical properties of full-thickness abdominal wall defects, either using Native tissues, with or without Overlay, and by substitution of the Defect by small intestinal submucosa mesh. METHODS: Seventy-two rats were divided into three groups according to repair method (Native, Overlay or Defect). At 7, 14, 30, and 90 days, six rats were sacrificed to measure tensile strength, collagen ingrowth, and host response. RESULTS: Explants had comparable strength at 30 days, the majority rupturing at the interface. Afterwards, the Native group was more resistant than both small intestine submucosa (SIS) groups with a more organized fibrotic scar on histology at 90 days. CONCLUSIONS: SIS augmentation of native tissue repair does not increase strength. Replacement of abdominal wall by SIS is equally strong when compared to the SIS-augmented group; however, materials preferably rupture at the site of the implant itself.