Nutrients inhibit gastric emptying in a dose-related fashion. We postulated that load-dependent gastric emptying results from the saturation of mucosal absorptive mechanisms, so that a longer length of the small intestine is exposed to unabsorbed nutrients as more nutrient enters the intestine to participate in this negative feedback. To test this idea, we limited exposure of 0.25 to 1.0 M glucose meals to various lengths of duodenum and jejunum in 17 dogs. The effects of these limited perfusions were then compared with experiments in which the whole gut (ALL) was exposed to the nutrient. Maximal inhibition was seen with 1.0 M meal and was similar with perfusions of 150 cm and ALL. By contrast, even with the 1.0 M load, no inhibition of gastric emptying was seen when glucose meal was confined to the first 15 cm of the proximal duodenum. Only 50-60% of maximal inhibition was observed during confinement of 1.0 M meal to the proximal 65 cm. We concluded that glucose sensors are present in both the proximal and the distal gut and the inhibition was related to the length of the small intestine exposed to glucose.
Substituted judgment by surrogates is not more accurate than random chance. Discussion between patient and surrogate about life support correlated with more accurate substituted judgment.
Ten parameters extracted from six currently used parametrizations of the four-parameter logistic model, and one new proposal, were examined for their statistical behavior in nonlinear least-squares estimation in combination with ELISA and RIA data. Those which are adequately near-linear on the basis of the Lowry-Morton lambda statistic were identified and can be recommended for use in practice.
Previously, we reported that inhibition of gastric emptying by glucose or acids depends on the length of gut exposed to the inhibitor [Gastroenterology 95: A877, 1988; Am. J. Physiol. 256 (Gastrointest. Liver Physiol. 19): G404-G411, 1989]. In this study, we hypothesized that feedback control by fat may be similarly regulated. In dogs with chronic intestinal fistulas, we compared the intensity of intestinal feedback when different lengths of the small intestine were exposed to meals of 3, 9, or 27 mM sodium oleate. We found that 1) inhibition of liquid emptying was dose dependent, 2) intensity of negative feedback was dependent on both the concentration of the oleate and the length of gut exposed to fat, 3) full inhibitory effect was achieved with exposure of fat to 150 cm of gut, 4) inhibition from the distal one-half of gut was less potent than that generated from the proximal one-half of gut, and 5) on a molar basis oleate was 20 times as effective as glucose at inhibition of gastric emptying and that this difference was related to the slower rate of fat absorption.
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