BACKGROUND & AIMS: The primary mechanism that originates symptoms in response to gastric distention remains undefined. The aim of this study was to determine which factor, whether intragastric volume, pressure, or wall tension, determines perception of gastric distention. METHODS: Healthy subjects underwent increasing gastric distentions (2-minute duration at 5-minute intervals) either at fixed pressure levels using a conventional barostat (n = 10) or at fixed tension levels using a newly developed computerized tensostat (n = 12); perception was scored by a 0-6 scale. Distentions were performed during basal conditions (intravenous saline) and during gastric relaxation by glucagon administration (4.8 microgram/kg intravenous bolus plus 9.6 microgram. kg-1. h-1 infusion). RESULTS: Isobaric distentions with the conventional barostat produced more intense perception during glucagon (95% +/- 40% higher; P < 0.05). However, the factor that determined higher perception could not be ascertained, because at the same pressure levels both intragastric volume and wall tension were greater during glucagon administration (174% +/- 56% and 34% +/- 8% greater, respectively; P < 0.05 vs. saline for both). The tensostat evidenced that perception was selectively related to tension, not to elongation; during glucagon administration, intragastric volumes were significantly larger (80% +/- 28% larger increase; P < 0.05), but perception of isotonic distentions remained the same (27% +/- 22%; nonsignificant change). CONCLUSIONS: Gastric wall tension, but not intragastric volume, determines perception of gastric distention, at least below nociception.
BACKGROUND & AIMS: The primary mechanism that originates symptoms in response to gastric distention remains undefined. The aim of this study was to determine which factor, whether intragastric volume, pressure, or wall tension, determines perception of gastric distention. METHODS: Healthy subjects underwent increasing gastric distentions (2-minute duration at 5-minute intervals) either at fixed pressure levels using a conventional barostat (n = 10) or at fixed tension levels using a newly developed computerized tensostat (n = 12); perception was scored by a 0-6 scale. Distentions were performed during basal conditions (intravenous saline) and during gastric relaxation by glucagon administration (4.8 microgram/kg intravenous bolus plus 9.6 microgram. kg-1. h-1 infusion). RESULTS: Isobaric distentions with the conventional barostat produced more intense perception during glucagon (95% +/- 40% higher; P < 0.05). However, the factor that determined higher perception could not be ascertained, because at the same pressure levels both intragastric volume and wall tension were greater during glucagon administration (174% +/- 56% and 34% +/- 8% greater, respectively; P < 0.05 vs. saline for both). The tensostat evidenced that perception was selectively related to tension, not to elongation; during glucagon administration, intragastric volumes were significantly larger (80% +/- 28% larger increase; P < 0.05), but perception of isotonic distentions remained the same (27% +/- 22%; nonsignificant change). CONCLUSIONS: Gastric wall tension, but not intragastric volume, determines perception of gastric distention, at least below nociception.