scholarly journals Serosal Surface of the Liver

2020 ◽  
Author(s):  
Keyword(s):  
Author(s):  
Rick L. Vaughn ◽  
Shailendra K. Saxena ◽  
John G. Sharp

We have developed an intestinal wound model that includes surgical construction of an ileo-cecal patch to study the complex process of intestinal wound healing. This allows approximation of ileal mucosa to the cecal serosa and facilitates regeneration of ileal mucosa onto the serosal surface of the cecum. The regeneration of ileal mucosa can then be evaluated at different times. The wound model also allows us to determine the rate of intestinal regeneration for a known size of intestinal wound and can be compared in different situations (e.g. with and without EGF and Peyer’s patches).At the light microscopic level it appeared that epithelial cells involved in regeneration of ileal mucosa originated from the enlarged crypts adjacent to the intestinal wound and migrated in an orderly fashion onto the serosal surface of the cecum. The migrating epithelial cells later formed crypts and villi by the process of invagination and evagination respectively. There were also signs of proliferation of smooth muscles underneath the migratory epithelial cells.


2011 ◽  
Vol 34 (9) ◽  
pp. 1514-1517 ◽  
Author(s):  
Toyoharu Mine ◽  
Hiroki Ishii ◽  
Sayuri Nakajima ◽  
Naoki Yoshikawa ◽  
Hirotaka Miyamoto ◽  
...  

1962 ◽  
Vol 203 (1) ◽  
pp. 73-80 ◽  
Author(s):  
James G. Manis ◽  
David Schachter

Everted gut sacs prepared from the proximal duodenum of the rat, mouse, and golden hamster can transfer iron actively, i.e. against concentration and potential gradients, from the mucosa to the serosa. The active transfer involves two steps: mucosal uptake and net transfer to the serosal surface. Oxidative metabolism is apparently required for each of the steps. Net transfer to the serosal surface is slower, more readily rate-limited, and more sharply localized to the proximal duodenum than is mucosal uptake. Both divalent and trivalent iron are taken up at the mucosal surface, but net transfer to the serosal surface is relatively specific for divalent iron. Calcium inhibits the net serosal transfer of iron at concentrations which do not inhibit the mucosal uptake. Parallel studies with loops of duodenum in living rats indicate that the active, two-step mechanism for iron absorption also functions in vivo, where the steps in the transfer are mucosal uptake followed by transport from the tissue to the blood stream.


1982 ◽  
Vol 243 (2) ◽  
pp. G117-G126
Author(s):  
R. Fogel ◽  
G. W. Sharp ◽  
M. Donowitz

The effects of chloroquine diphosphate, a drug with "'membrane-stabilizing" properties, were studied on basal ileal absorption and on ileal secretion induced by increased intracellular cAMP levels and calcium (serotonin). The studies were performed on rat (in vivo) and rabbit ileum (in vitro). Intraluminal chloroquine (10(-4) M) reversed cholera toxin- and theophylline-induced secretion in rat ileum but did not alter the cholera toxin- and theophylline-induced increases in cAMP content. Addition of chloroquine (10(-4) M) to the mucosal surface of rabbit ileum did not alter basal active electrolyte transport or the serotonin-induced decreased Na and Cl absorption but inhibited the theophylline-induced C1 secretion. Addition of chloroquine (10(-4)) M) to the serosal surface stimulated net Na and Cl absorption. This effect may involve intracellular calcium. Chloroquine increased the rabbit ileal calcium content and decreased 45Ca2+ influx from the serosal surface. Both the mucosal and serosal effects of chloroquine described led to a net increase in absorptive function of the intestine and should prove useful in developing treatment of diarrheal diseases.


1965 ◽  
Vol 208 (3) ◽  
pp. 528-530 ◽  
Author(s):  
Horace W. Davenport ◽  
Peter H. Abbrecht

Frog gastric mucosa was formed into a sac, filled with 1 ml salt solution and incubated in a large volume of identical salt solution containing 3 mm potassium and K42. Total potassium and specific activities of tissue and fluid were measured at 5, 10, 20, 40, 80, and 160 min after start of incubation. The measurements were repeated on mucosas formed into sacs with the mucosal side out. Both types of sacs were also incubated in solutions containing 0.1 mm histamine. Results confirm observations of others that there is net movement of potassium from fluid bathing the serosal surface into the tissue and mucosal fluid and that histamine stimulates potassium movement from tissue into mucosal fluid. The data were used to calculate the ratio of the rate of movement of potassium across the serosal and mucosal surfaces, Rs/Rm. The numerical value of 4.72 was obtained without histamine and 7.16 with histamine.


1985 ◽  
Vol 249 (1) ◽  
pp. H155-H163 ◽  
Author(s):  
C. L. Stebbins ◽  
R. C. Smith ◽  
J. C. Longhurst

We examined the effect of prostaglandins on the reflex cardiovascular response to bradykinin applied to the abdominal organs of anesthetized cats. Bradykinin (10 micrograms/ml) was applied to the serosal surface of the stomach, gallbladder, or jejunum before and after injection of indomethacin (2-10 micrograms/ml iv) and after application of 1 microgram/ml of prostaglandins E1, E2, or F2 alpha (PGE1, PGE2, PGF2 alpha) or prostacyclin (PGI2). In six cats, stimulation of the stomach with bradykinin significantly increased mean arterial pressure (MAP) by 37 +/- 5 (SE) mmHg and maximal dP/dt by 633 +/- 101 mmHg/s. Following indomethacin the bradykinin-induced increases in MAP and dP/dt were significantly reduced to 19 +/- 4 mmHg and 191 +/- 58 mmHg/s, respectively. Treatment with PGE1, PGE2, or PGI2, but not PGF2 alpha, restored the initial bradykinin response. The gallbladder and jejunum responded similarly. Also application of exogenous prostaglandins, PGE2 or PGI2, to the stomach, gallbladder, or jejunum significantly augmented the cardiovascular response to bradykinin. Finally, PGE2 restored a portion of the cardiovascular response to bradykinin following the development of tachyphylaxis. We conclude that prostaglandins are necessary for the full manifestation of the cardiovascular response to bradykinin.


1983 ◽  
Vol 245 (2) ◽  
pp. G201-G207
Author(s):  
H. Nagata ◽  
P. H. Guth

The effect of histamine on gastric microvascular permeability to macromolecules in the rat was studied using fluorescent in vivo microscopy. Histamine was applied topically to the serosal surface for study of the muscularis externa, to the submucosa, and to the superficial mucosa, and the area of leaks of a fluorescein-albumin conjugate from microvessels was quantitated. In the muscularis externa both histamine and an H1-agonist, but not an H2-agonist, caused dose-dependent leak of conjugate from venules. An H1-antagonist, but not an H2-antagonist, decreased the histamine-induced leak. In the submucosa histamine caused dose-dependent dilatation of arterioles but not leak of conjugate. In contrast, bradykinin caused both dose-dependent dilatation of arterioles and leak of conjugate from venules. In the superficial mucosa histamine did not cause any leak. In conclusion, topical histamine 1) increased microvascular permeability to macromolecules from venules in the muscularis externa via H1-receptors, 2) did not affect microvascular permeability in the submucosa (this may be due to lack of histamine receptors on the venules as bradykinin increased venular permeability), and 3) did not affect microvascular permeability in the superficial mucosa, but there might not have been adequate histamine backdiffusion.


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