The Patterns of Simultaneous Intraluminal Pressure Changes in the Human Proximal Small Intestine

1964 ◽  
Vol 47 (3) ◽  
pp. 258-268 ◽  
Author(s):  
Gerald Friedman ◽  
Jerome D. Waye ◽  
Leonard A. Weingarten ◽  
Henry D. Janowitz
2002 ◽  
Vol 132 (9) ◽  
pp. 2713-2716 ◽  
Author(s):  
Randal K. Buddington ◽  
Karyl K. Buddington ◽  
Dong-Fang Deng ◽  
Gro-Ingunn Hemre ◽  
Robert P. Wilson

1999 ◽  
Vol 276 (5) ◽  
pp. G1195-G1203 ◽  
Author(s):  
David M. Hall ◽  
Kirk R. Baumgardner ◽  
Terry D. Oberley ◽  
Carl V. Gisolfi

Exposure of conscious animals to environmental heat stress increases portal venous radical content. The nature of the observed heat stress-inducible radical molecules suggests that hyperthermia produces cellular hypoxic stress in liver and intestine. To investigate this hypothesis, conscious rats bearing in-dwelling portal venous and femoral artery catheters were exposed to normothermic or hyperthermic conditions. Blood gas levels were monitored during heat stress and for 24 h following heat exposure. Hyperthermia significantly increased arterial O2saturation, splanchnic arterial-venous O2difference, and venous[Formula: see text], while decreasing venous O2saturation and venous pH. One hour after heat exposure, liver glycogen levels were decreased ∼20%. Two hours after heat exposure, the splanchnic arterial-venous O2difference remained elevated in heat-stressed animals despite normal Tc. A second group of rats was exposed to similar conditions while receiving intra-arterial injections of the hypoxic cell marker [3H]misonidazole. Liver and intestine were biopsied, and [3H]misonidazole content was quantified. Heat stress increased tissue [3H]misonidazole retention 80% in the liver and 29% in the small intestine. Cellular [3H]misonidazole levels were significantly elevated in intestinal epithelial cells and liver zone 2 and 3 hepatocytes and Kupffer cells. This effect was most prominent in the proximal small intestine and small liver lobi. These data provide evidence that hyperthermia produces cellular hypoxia and metabolic stress in splanchnic tissues and suggest that cellular metabolic stress may contribute to radical generation during heat stress.


1986 ◽  
Vol 250 (4) ◽  
pp. G469-G474
Author(s):  
D. Hollander ◽  
E. M. Gerard ◽  
C. A. Boyd

Butyric acid transport was studied in the isolated, vascularly perfused frog small intestine. At luminal butyric acid concentrations of 5-50 mM, absorption was a nonlinear function of the luminal concentration, whereas the relationship of absorption to concentration remained linear at 0-1,000 microM. The most important factor regulating the rate and direction of butyric acid transport was the pH. We used unidirectional flux analysis to determine net transport across the epithelium while the pH of the luminal or vascular compartments was changed. We found a four- to fivefold decrease in butyric acid transport into the portal circulation as the lumen pH was increased from 6.0 to 8.0. The pH of the vascular perfusate influenced the vascular-to-lumen transport of butyric acid in the same proportions. The second important regulatory factor of butyric acid transport was the 4,4'-diisothiocyananostilbene-2,2'-disulfonic acid (DIDS)-sensitive anion transport protein. DIDS added to the lumen at 10(-6) M decreased butyric acid transport by approximately 40% at pH 7.4. DIDS also inhibited butyric acid transport when added to the vascular perfusate or when transport was measured in a vascular-to-lumen direction. We suggest that, at the relatively low pH of the proximal small intestine, butyric acid becomes protonated and lipophilic and is mainly transported directly through the cell membrane. At the more alkaline pH of the distal small intestine butyric acid is in the ionized form and transport by the DIDS-sensitive anion transport protein may predominate.


1960 ◽  
Vol 199 (3) ◽  
pp. 589-592 ◽  
Author(s):  
Paul C. Johnson

The purpose of these experiments was to study the changes in intestinal volume occurring with hemorrhage, utilizing a gravimetric technique which permitted a study of small segments of the intestine. It had been observed previously that intestinal weight often increased in the upper small intestine during hemorrhage, while in the lower small intestine it usually decreased. In studying the latter effect it was found that sympathetic nerve activity and reduction of venous pressure were both important in decreasing intestinal volume. Changes in tonus and local reduction in arterial pressure did not appear to be important. The increase in volume with hemorrhage appeared due to epinephrine discharge from the adrenal medulla since it was eliminated by adrenalectomy. Local pressure changes and alteration of tonus were eliminated as causal factors. It appears that systemic hypotension induces sympathetic discharge which in turn may cause either an increase or a decrease in intestinal blood volume. Sympathetic discharge over the vasoconstrictor fibers reduces blood volume while adrenal medullary secretion increases it. The observed response is apparently a resultant of these two antagonistic effects.


1990 ◽  
Vol 259 (1) ◽  
pp. G78-G85 ◽  
Author(s):  
M. L. Siegle ◽  
H. R. Schmid ◽  
H. J. Ehrlein

In the present study, effects of ileal infusions of nutrients on motor patterns of the proximal small intestine and on gastric emptying were investigated in dogs. An acaloric meal was administered orally, and equicaloric loads of amino acids, oleate, and glucose were infused into the ileum at different doses (0.3, 0.6, and 0.9 kJ/min). The computerized analysis of motor patterns was focused on the differentiation between stationary and propagated contractions recorded by closely spaced extraluminal strain gauges. All three nutrients exerted inhibitory effects on gastric emptying and on contraction force and frequency of the proximal small intestine. Additionally, the propulsive motor pattern induced by the acaloric meal was modulated by reducing the number of contraction waves and their length of spread. All the effects were dose dependent. Among the three nutrients, glucose significantly changed motility at lower doses compared with amino acids and oleate. We conclude that in dogs the ileal brake mechanism is induced by all three nutrients and that it influences not only contraction force and frequency but also the motor patterns of the proximal small intestine.


1988 ◽  
Vol 255 (6) ◽  
pp. G813-G817 ◽  
Author(s):  
J. G. Wood ◽  
H. D. Hoang ◽  
L. J. Bussjaeger ◽  
T. E. Solomon

Neurotensin has many actions on digestive tract motility and secretion and stimulates pancreatic growth. We examined effects of chronic administration of neurotensin on growth of small intestine and colon. Four groups of 10 rats were injected with saline or neurotensin (33, 100, or 300 micrograms/kg) every 8 h for 5 days. The small intestine was divided into four segments of equal length, weighed, and assayed for DNA, protein, and brush-border digestive enzymes. The colon was weighed and assayed for DNA and protein. Neurotensin caused dose-related increases in growth of small intestine; at the highest dose, similar increases in weight (12-20%), DNA (23-35%), and protein content (33-39%) occurred in each segment of small intestine. Maltase, sucrase, and leucine aminopeptidase (but not lactase) contents were also significantly increased after neurotensin, but the largest effects were seen in the proximal small intestine. Neurotensin had no effect on weight, DNA, or protein content of the colon. These results suggest a role for neurotensin in regulating growth of small intestine.


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