scholarly journals Changes in Messenger RNA of Pancreatic Enzymes and Intestinal Cholecystokinin after a 7-Day Bile-pancreatic Juice Diversion from the Proximal Small Intestine in Rats

1997 ◽  
Vol 61 (6) ◽  
pp. 1002-1006
Author(s):  
Hiroshi Hara ◽  
Yasuo Ochi ◽  
Takanori Kasai
Keyword(s):  
Small Intestine ◽  
Pancreatic Juice ◽  
Messenger Rna ◽  
Pancreatic Enzymes ◽  
Proximal Small Intestine

Distribution and fate of pancreatic enzymes in small intestine of the rat

1962 ◽  
Vol 202 (2) ◽  
pp. 285-288 ◽  
Author(s):  
Daniel Pelot ◽  
Morton I. Grossman
Keyword(s):  
Small Intestine ◽  
Pancreatic Juice ◽  
Pancreatic Enzymes ◽  
The Body ◽  
Intact Rats

The trypsin, chymotrypsin, and lipase activities of washings of the small intestine of the rat were measured. Diversion of pancreatic juice to the exterior of the body resulted in rapid disappearance of enzymes from the small intestine with virtually complete absence after 16 hr. For all three enzymes, larger amounts were present in the lower than in the upper half of the small intestine. By several criteria the order of rate of inactivation, from least to most rapid, was trypsin, chymotrypsin, and lipase. Feces of intact rats contained readily measurable amounts of all three of these enzymes.

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
Keyword(s):  
Small Intestine ◽  
Intraluminal Pressure ◽  
Proximal Small Intestine ◽  
Pressure Changes

scholarly journals A High Retinol Dietary Intake Increases its Apical Absorption by the Proximal Small Intestine of Juvenile Sunshine Bass (Morone chrysops × M. saxatilis)

2002 ◽  
Vol 132 (9) ◽  
pp. 2713-2716 ◽  
Author(s):  
Randal K. Buddington ◽  
Karyl K. Buddington ◽  
Dong-Fang Deng ◽  
Gro-Ingunn Hemre ◽  
Robert P. Wilson
Keyword(s):  
Small Intestine ◽  
Dietary Intake ◽  
Morone Chrysops ◽  
Sunshine Bass ◽  
Proximal Small Intestine

Tissue Factor Expression in Vital Organs during Murine Traumatic Shock 

1999 ◽  
Vol 91 (6) ◽  
pp. 1844-1844 ◽  
Author(s):  
Valerie E. Armstead ◽  
Irina L. Opentanova ◽  
Alexander G. Minchenko ◽  
Allan M. Lefer
Keyword(s):  
Small Intestine ◽  
Mrna Expression ◽  
Tissue Factor ◽  
Messenger Rna ◽  
Mrna Level ◽  
Regulatory Elements ◽  
Traumatic Shock ◽  
Surface Glycoprotein ◽  
Cell Surface Glycoprotein ◽  
Nf Kappab

Background Tissue factor (TF) is a cell-surface glycoprotein responsible for initiating the extrinsic pathway of coagulation that has been shown to have a role in the pathophysiology of sepsis and reperfusion injury. The purpose of this study was to investigate TF expression in vital organs and to determine possible regulatory mechanisms of TF expression in the lung during traumatic shock in rats. Methods Noble-Collip drum trauma was induced in anesthetized Sprague-Dawley rats. Anesthetized rats without trauma served as controls. TF activity was measured in plasma and lung tissue. TF messenger RNA (mRNA) was measured in the lung, liver, and small intestine using ribonuclease protection assays. Electromobility shift assays were used to quantify binding of nuclear extracts from lung to TF-specific consensus domains for transcription factors NF-kappaB and AP-1. Results TF activity in plasma increased up to 14-fold and +232% in the lung (P < 0.001 for plasma and lung) 2 h after trauma. TF mRNA level was significantly increased in the lungs (P < 0.01), small intestine (P < 0.01), and liver (P < 0.05) 1 h after trauma compared to sham-operated control rats. TF mRNA expression continued to increase in the lungs and the liver (both, P < 0.001) 2 h after trauma TF sequence-specific complex binding to AP-1 and NF-kappaB domains was enhanced in the lungs of trauma rats (+395%, P < 0.001 and +168%, P < 0.001, respectively). Conclusions These results suggest that TF may play an important role in the pathophysiology of severe trauma and that regulatory elements AP-1 and NF-kappaB may be involved in the regulation of TF mRNA expression in traumatic shock.

Splanchnic tissues undergo hypoxic stress during whole body hyperthermia

1999 ◽  
Vol 276 (5) ◽  
pp. G1195-G1203 ◽  
Author(s):  
David M. Hall ◽  
Kirk R. Baumgardner ◽  
Terry D. Oberley ◽  
Carl V. Gisolfi
Keyword(s):  
Small Intestine ◽  
Heat Stress ◽  
Heat Exposure ◽  
Metabolic Stress ◽  
Liver Glycogen ◽  
Whole Body ◽  
Hypoxic Cell ◽  
Hypoxic Stress ◽  
Proximal Small Intestine ◽  
Radical Content

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.

Adaptation to fat markedly increases pancreatic secretory response to intraduodenal fat in rats

1996 ◽  
Vol 270 (1) ◽  
pp. G128-G135 ◽  
Author(s):  
A. W. Spannagel ◽  
I. Nakano ◽  
T. Tawil ◽  
W. Y. Chey ◽  
R. A. Liddle ◽  
...  
Keyword(s):  
Small Intestine ◽  
Pancreatic Juice ◽  
Lipolytic Activity ◽  
Exocrine Secretion ◽  
Secretory Response ◽  
Pancreatic Exocrine Secretion ◽  
High Fat ◽  
Functional Consequences ◽  
Pancreatic Exocrine ◽  
Cck Release

Exposure to higher levels of fat in the diet increases the secretion of fat-digesting enzymes in pancreatic juice. This study examines the functional consequences of this phenomenon and demonstrates that adapting rats to high fat (triglyceride) loads increases the release of cholecystokinin (CCK) and the pancreatic secretory response to intraduodenal fat. Lipolytic activity in the small intestine was also higher in adapted rats. Exchanging pancreatic juice from unadapted rats with pancreatic juice from adapted rats decreased the response to fat in adapted rats and increased the response to fat in unadapted rats. Infusing oleic acid into unadapted rats stimulated CCK secretion and pancreatic exocrine secretion to levels observed with triglycerides in adapted rats. Pancreatic exocrine secretion in response to intraduodenal fat in rats adapted to a high-fat (20%) diet were significantly higher than the responses seen in rats fed a low-fat (5%) diet. Adaptation to fat increases the pancreatic secretory and plasma CCK responses to fat, apparently by increasing the efficiency of triglyceride digestion and thereby increasing CCK release.

Transport of butyric acid in vascularly perfused anuran small intestine: importance of pH and anion transport

1986 ◽  
Vol 250 (4) ◽  
pp. G469-G474
Author(s):  
D. Hollander ◽  
E. M. Gerard ◽  
C. A. Boyd
Keyword(s):  
Small Intestine ◽  
Butyric Acid ◽  
Nonlinear Function ◽  
Anion Transport ◽  
Transport Protein ◽  
Disulfonic Acid ◽  
Flux Analysis ◽  
Acid Transport ◽  
Distal Small Intestine ◽  
Proximal Small Intestine

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.

Sign in / Sign up

Export Citation Format

Share Document