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- Holm-Rutili, Lena
(author)
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Effects of omeprazole on gastric mucosal microcirculation and acid secretion in the rat
- 1987
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In: Gastroenterology. - 0016-5085 .- 1528-0012. ; 92:3, s. 716-723
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Journal article (peer-reviewed)abstract
- Omeprazole, a potent long-acting inhibitor of gastric acid secretion that exerts its inhibitory action by direct blocking of the H+, K+-adenosine triphosphatase in the parietal cells, was either applied topically to the solution bathing the exposed mucosa of the test rats or administered intravenously as a bolus injection. The superficial mucosal vessels were monitored on a television screen through a microscope and videorecorded for off-line analysis of red cell velocities and vessel diameters, from which blood flow was calculated. Intravenous omeprazole (5 or 10 mumol/kg) totally abolished the basal secretion 15-25 min after injection, with a parallel decrease in blood flow of approximately 25% for both doses. Omeprazole, 5 mumol/kg, given intravenously to rats stimulated with pentagastrin (20 micrograms/kg X h) significantly inhibited the stimulated acid output, but the blood flow was not significantly decreased. Topical application of omeprazole (2.5 mM in 6 ml) significantly increased blood flow (approximately 15%) while in contact with the mucosa both in the resting and in the pentagastrin (20 micrograms/kg X h)-stimulated situations. However, 10-20 min after the application period, blood flow was restored to the values before application of omeprazole and the acid output was significantly decreased. The results indicate that omeprazole exerts only minor influences on the gastric mucosal microcirculation in spite of its potent acid-inhibitory effect.
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- Smith, S M, et al.
(author)
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Role of neutrophils in hemorrhagic shock-induced gastric mucosal injury in the rat
- 1987
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In: Gastroenterology. - 0016-5085 .- 1528-0012. ; 93:3, s. 466-471
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Journal article (peer-reviewed)abstract
- Gastric mucosal clearance of 51Cr-labeled red blood cells (51Cr-RBC) was measured in rats during a 30-min control period, a 30-min ischemic period (hemorrhage to 27 mmHg arterial pressure), and a 60-min reperfusion period (reinfusion of shed blood). In untreated (control) rats, a dramatic rise in the leakage of 51Cr-labeled red blood cells into the gastric lumen was observed during the reperfusion period. Treatment with neutrophil antiserum attenuated 51Cr-labeled red blood cell flux into the gastric lumen. Using the radioactive microsphere technique, neutrophil-depleted animals were shown to have higher blood flows in the ischemic period than the untreated rats. Bleeding of untreated rats to a mean arterial pressure of 40 mmHg resulted in blood flows that were not different from those in antiserum-treated rats bled to 27 mmHg and leakage of 51Cr-labeled red blood cells similar to that measured in antiserum-treated rats. The results of this study indicate that neutrophils play an important role in hemorrhagic shock-induced gastric bleeding.
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