Modulatory Role of 5-HT3 Receptors in Gastric Function and Ethanol·lnduced Mucosal Damage in Rat Stomachs

Pharmacology ◽  
1994 ◽  
Vol 49 (3) ◽  
pp. 137-143 ◽  
Author(s):  
C.H. Cho ◽  
M.W.L. Koo ◽  
J.K.S. Ko
Keyword(s):  
Mucosal Damage ◽  
Gastric Function

Aspirin-induced changes in gastric function: Role of endogenous prostaglandins and mucosal damage

1990 ◽  
Vol 98 (2) ◽  
pp. 284-292 ◽  
Author(s):  
Terez Shea-Donohue ◽  
Linda Steel ◽  
Elizabeth Montcalm-Mazzilli ◽  
Andre Dubois
Keyword(s):  
Mucosal Damage ◽  
Gastric Function ◽  
Endogenous Prostaglandins ◽  
Induced Changes

scholarly journals Role of Dietary Nutritional Treatment on Hepatic and Intestinal Damage in Transplantation with Steatotic and Non-Steatotic Liver Grafts from Brain Dead Donors

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2554
Author(s):  
Marc Micó-Carnero ◽  
Araní Casillas-Ramírez ◽  
Albert Caballeria-Casals ◽  
Carlos Rojano-Alfonso ◽  
Alfredo Sánchez-González ◽  
...  
Keyword(s):  
Growth Factor ◽  
Gut Microbiota ◽  
Intestinal Inflammation ◽  
Mucosal Damage ◽  
Hepatic Damage ◽  
Intestinal Damage ◽  
Edema Formation ◽  
Steatotic Liver ◽  
Damage And Failure

Herein, we investigate whether: (1) the administration of glucose or a lipid emulsion is useful in liver transplantation (LT) using steatotic (induced genetically or nutritionally) or non-steatotic livers from donors after brain death (DBDs); and (2) any such benefits are due to reductions in intestinal damage and consequently to gut microbiota preservation. In recipients from DBDs, we show increased hepatic damage and failure in the maintenance of ATP, glycogen, phospholipid and growth factor (HGF, IGF1 and VEGFA) levels, compared to recipients from non-DBDs. In recipients of non-steatotic grafts from DBDs, the administration of glucose or lipids did not protect against hepatic damage. This was associated with unchanged ATP, glycogen, phospholipid and growth factor levels. However, the administration of lipids in steatotic grafts from DBDs protected against damage and ATP and glycogen drop and increased phospholipid levels. This was associated with increases in growth factors. In all recipients from DBDs, intestinal inflammation and damage (evaluated by LPS, vascular permeability, mucosal damage, TLR4, TNF, IL1, IL-10, MPO, MDA and edema formation) was not shown. In such cases, potential changes in gut microbiota would not be relevant since neither inflammation nor damage was evidenced in the intestine following LT in any of the groups evaluated. In conclusion, lipid treatment is the preferable nutritional support to protect against hepatic damage in steatotic LT from DBDs; the benefits were independent of alterations in the recipient intestine.

Role of Lipoxygenases and the Lipoxin A4/Annexin 1 Receptor in Ischemia-Reperfusion-Induced Gastric Mucosal Damage in Rats

Pharmacology ◽  
2009 ◽  
Vol 84 (5) ◽  
pp. 294-299 ◽  
Author(s):  
Brigitta M. Peskar ◽  
Karlheinz Ehrlich ◽  
Rufina Schuligoi ◽  
Bernhard A. Peskar
Keyword(s):  
Ischemia Reperfusion ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Lipoxin A4 ◽  
Annexin 1

Role of Prostaglandins in Bile Salt-Induced Changes in Rat Colonic Structure and Function

1981 ◽  
Vol 61 (5) ◽  
pp. 641-648 ◽  
Author(s):  
D. S. Rampton ◽  
N. F. Breuer ◽  
S. G. Vaja ◽  
G. E. Sladen ◽  
R. H. Dowling
Keyword(s):  
Bile Salt ◽  
Goblet Cell ◽  
Tissue Damage ◽  
Mucosal Damage ◽  
Cell Depletion ◽  
Sodium Absorption ◽  
Perfusion Fluid ◽  
Synthesis Inhibitor ◽  
Induced Changes

1. The role of prostaglandins in mediating bile salt-induced diarrhoea was investigated with a colonic perfusion technique in vivo in rats either untreated or pretreated with the prostaglandin (PG) synthesis inhibitor, indomethacin. 2. Colonic perfusion with sodium deoxycholate (1 and 2 mmol/l) reduced net water and sodium absorption, whereas at a concentration of 5 mmol/l it caused net fluid secretion. Deoxycholate dose-dependently increased protein and deoxyribonucleic acid (DNA) output into the perfusion fluid and, at a concentration of 5 mmol/l, produced histological evidence of colonic mucosal damage (mucus release, goblet cell depletion, patchy epitheliolysis and inflammatory cell infiltration); histological change was less with deoxycholate at 2 mmol/l and did not occur at 1 mmol/l. 3. Output of immunoreactive prostaglandin E2 (PGE2) into the colonic perfusion fluid rose eight-, 10- and 270-fold after deoxycholate at 1, 2 and 5 mmol/l respectively. 4. Colonic perfusion with added PGE2, in concentrations 10 times lower (2.8 nmol/l) and 10 times higher (0.28 μmol/l) than those found in the perfusate after deoxycholate at 5 mmol/l did not alter mucosal function or structure. However, PGE2 in much higher concentration (0.28 mmol/l) reduced net absorption of water and sodium, increased protein output threefold and, as seen with light microscopy, produced excess surface mucus with minimal goblet cell depletion and no tissue damage. 5. Pretreatment with indomethacin reduced the colonic PGE2 output of rats perfused with deoxycholate at 2 and 5 mmol/l by 56 and 87% respectively, but the bile salt-induced changes in net water and sodium transport and DNA output were not significantly affected. The PG synthesis inhibitor reduced protein loss, goblet cell depletion and surface mucus seen after perfusion with deoxycholate at 2 mmol/l, although it did not prevent the more marked structural changes caused by deoxycholate at 5 mmol/l. 6. These results suggest that in rats prostaglandins (i) are not important mediators of the deoxycholate-induced impairment of colonic water and electrolyte transport, (ii) may contribute to the mucus secretion and goblet cell depletion produced by perfusion with deoxycholate in concentrations below those causing gross tissue damage, and that (iii) overt mucosal damage is not an essential prerequisite for prostaglandin release.

scholarly journals Role of taurocholic acid in production of gastric mucosal damage after ingestion of aspirin.

BMJ ◽  
1975 ◽  
Vol 1 (5951) ◽  
pp. 183-185 ◽  
Author(s):  
K M Cochran ◽  
J F Mackenzie ◽  
R I Russell
Keyword(s):  
Mucosal Damage ◽  
Taurocholic Acid ◽  
Gastric Mucosal Damage
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