Differences in action of topical and systemic cysteamine on gastric blood flow, gastric acid secretion and gastric ulceration in the rat

1996 ◽  
Vol 90 (2) ◽  
pp. 63-73 ◽  
Author(s):  
O.M.E Abdel-Salam ◽  
J Szolcsányi ◽  
G Mózsik
1989 ◽  
Vol 256 (1) ◽  
pp. G145-G149 ◽  
Author(s):  
P. Bauerfeind ◽  
R. Hof ◽  
A. Hof ◽  
M. Cucala ◽  
S. Siegrist ◽  
...  

Effects of intravenously administered human calcitonin gene-related peptides (hCGRP) I and II on regional blood flow and gastric acid secretion were examined in barbiturate-anesthetized rabbits. Blood flow was measured by injection of radioactively labeled microspheres at 0, 10, 20, 30, and 60 min. hCGRP I and II and vehicle were infused intravenously in five rabbits in rising doses of 0.01 (0-10th min), 0.03 (11-20th min), and 0.1 microgram.kg-1.min-1 (21-30th min). hCGRP I and II increased gastric blood flow dose dependently. Moreover, hCGRP I raised regional conductance (inverse of vascular resistance) in the stomach, duodenum, heart, brain, and skeletal muscle. As a result of the increased total peripheral conductance the mean arterial pressure was reduced, but the cardiac output remained unchanged. hCGRP II increased blood flow and conductance selectively in the stomach and the pancreas. The total peripheral conductance and mean arterial pressure remained unchanged. Apparently, hCGRP II exerts a more localized effect on the stomach than hCGRP I. hCGRP I and II did not affect basal gastric acid secretion. Pentagastrin-stimulated acid secretion was increased by 28% with hCGRP I (0.025 micrograms.kg-1.min-1) and decreased by 27% with hCGRP II (0.025 micrograms.kg-1.min-1). The inverse effect of hCGRP I and II and the parallel stimulation of blood flow brought about with hCGRP I and II indicate a different mode of action of the peptides on gastric blood flow and gastric acid secretion.


1988 ◽  
Vol 95 (3) ◽  
pp. 642-650 ◽  
Author(s):  
Josep M. Pique ◽  
Felix W. Leung ◽  
Heck W. Tan ◽  
Edward Livingston ◽  
Oscar U. Scremin ◽  
...  

1993 ◽  
Vol 71 (10-11) ◽  
pp. 829-834 ◽  
Author(s):  
Lynn E. Hierlihy ◽  
John L. Wallace ◽  
Alastair V. Ferguson

Vagal stimulation has been shown to result in the development of gastric mucosal erosions in the rat, although the mechanisms underlying the development of such erosions are not known. The effects of vagal stimulation on gastric acid secretion and mucosal blood flow were examined in urethane-anesthetized male Sprague–Dawley rats to determine whether changes in these factors correlate with the mucosal damage in response to vagal stimulation. Electrical stimulation (5 Hz, 5 V, 1 ms for 60 min) of afferent or efferent components of the vagi was not found to induce any significant increase in the mean acid secretory rate compared with control animals (p > 0.05). In contrast, stimulation of intact vagus nerves induced a significant increase in the mean acid secretory rate compared with control and efferent- and afferent-stimulated groups (p < 0.01). Measurement of gastric blood flow with laser-Doppler flowmetry demonstrated intact vagal stimulation to have no significant effect on gastric blood flow. These data suggest that such vagal stimulation induced increases in acid secretion in urethane-anesthetized animals may represent a part of the integrated physiological response to such stimulation which leads to the development of gastric mucosal erosions within 60 min. Pretreatment with antisecretory agents such as cimetidine and inter-leukin-1β significantly reduce the gastric mucosal injury compared with untreated animals (p < 0.05), emphasizing the important role of acid secretion in the development of vagal-induced gastric damage.Key words: vagus, acid secretion, blood flow, gastric.


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