Rat gastric mucosal microcirculation in vivo

The superficial gastric mucosal microcirculation was observed microscopically by transillumination in the anesthetized rat. The vessels surrounding the gastric crypts were monitored on a television screen through a microscope and the pictures stored on a videotape for off-line analysis of red cell velocity (VRBC) and vessel diameter. From these measurements microvascular volume flows were calculated. VRBC reached steady values after 1-4 h (mean 2 h) and showed a regular pulsatile flow (4-7 cycles/min) in most experiments. Acid output was measured at regular intervals; 50% of the rats showed no spontaneous acid output, but the others secreted up to 100 mu eq/h. The microvessels in the superficial mucosa were classified into three orders according to their branching hierarchy and relative dimensions, and their distribution per unit mass was estimated. VRBC and volume flow were shown to decrease in the successive orders of the microvessels. Calculation of organ blood flow from microvascular flow data and vessel distribution gave values (21 ml.min-1.100 g tissue-1) that agree with earlier reported values. A higher flow velocity was detected in rats with spontaneous acid output than in those without, but there was a poor correlation between the magnitude of the acid output and VRBC. Pentagastrin (96 micrograms.kg-1.h-1) induced a significant increase in both blood flow and acid secretion. Results from this study indicate that this experimental model is potentially useful for studies of the correlation between acid secretion and mucosal blood flow.

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Effect of xenopsin on blood flow, hormone release, and acid secretion

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1982.243.3.g195 ◽

1982 ◽

Vol 243 (3) ◽

pp. G195-G199 ◽

Cited By ~ 1

Author(s):

M. J. Zinner ◽

F. Kasher ◽

I. M. Modlin ◽

B. M. Jaffe

Keyword(s):

Blood Flow ◽

Acid Secretion ◽

Gastric Acid ◽

Regional Blood Flow ◽

Acid Output ◽

Significant Inhibition ◽

Organ Blood Flow ◽

Hormone Release ◽

Change In Mean ◽

Specific Influence

We investigated the effects of the neurotensin analogue xenopsin on regional blood flow, central hemodynamics, and stimulated acid secretion in awake conscious dogs. Organ blood flow, estimated using the radioactive microsphere technique, was significantly increased during the xenopsin infusion to the adrenals, pancreas, and ileum. There was no change in mean arterial pressure or cardiac output (measured by thermodilution). Along with changes in blood flow, there was a significant increase in the hormone output from the pancreas. These included rises in plasma pancreatic polypeptide, insulin, and glucagon. There also was a rise in plasma cortisol levels during the infusion. Substance P levels rose slowly but significantly during the xenospin infusion. There was no change in plasma gastrin levels. Xenopsin produced a significant inhibition of tetragastrin-stimulated gastric acid output. Thus, xenopsin appears to have region-specific influence on blood flow that correlates with region-specific hormonal secretion. In addition, xenopsin, like its mammalian analogue neurotensin, is an inhibitor of stimulated gastric acid secretion. A mammalian xenopsinlike peptide may well be involved in the modulation of gastrointestinal function.

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Pentagastrin enhances gastric mucosal defenses in vivo: luminal acid-dependent and independent effects

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1994.267.1.g94 ◽

1994 ◽

Vol 267 (1) ◽

pp. G94-G104 ◽

Cited By ~ 4

Author(s):

Y. Nishizaki ◽

P. H. Guth ◽

G. Kim ◽

H. Wayland ◽

J. D. Kaunitz

Keyword(s):

Blood Flow ◽

Acid Secretion ◽

Defense Mechanisms ◽

Mucosal Blood Flow ◽

Gastric Mucosal Blood Flow ◽

H2 Receptor Antagonist ◽

Protective Mechanisms ◽

Mucus Gel ◽

Increased Blood Flow

Stimulation of acid secretion is associated with enhanced resistance of the gastric mucosa to damage by luminal acid. We studied the mechanism by which gastric mucosal defenses are modulated in a system in which mucus gel thickness, intracellular pH (pHi), gastric mucosal blood flow, and acid secretion can be measured simultaneously in vivo, using a recently developed microfluorometric technique. Intravenous infusion of pentagastrin in a dose associated with maximal acid secretion increased mucus gel thickness, pHi, and mucosal blood flow during superfusion with a neutral solution. Subsequent superfusion with an acidic buffer (pH 1.7) further increased blood flow to nearly three times basal. During superfusion with luminal acid, pHi fell more slowly and recovered toward baseline more quickly in pentagastrin-infused rats than in controls. Pretreatment with the H2-receptor antagonist cimetidine abolished the increased blood flow associated with pentagastrin, impairing pHi homeostasis, although cimetidine increased mucus gel thickness in the absence of pentagastrin. We conclude that gastric defense mechanisms at the preendothelial and postepithelial levels are enhanced during acid secretion as part of a histamine-dependent homeostatic mechanism that balances gastric protective mechanisms with acid secretion. The net result of these enhanced defenses is the preservation of gastric surface cell pHi despite the presence of a large proton gradient between lumen and blood.

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Dissociated effects of somatostatin on gastric acid secretion and mucosal blood flow

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1985.248.3.g337 ◽

1985 ◽

Vol 248 (3) ◽

pp. G337-G341

Author(s):

F. W. Leung ◽

P. H. Guth

Keyword(s):

Blood Flow ◽

Acid Secretion ◽

Gastric Acid Secretion ◽

Gastric Acid ◽

Acid Output ◽

Mucosal Blood Flow ◽

Hydrogen Gas ◽

Gastric Acid Output ◽

Hydrogen Gas Clearance ◽

Blood Flows

Somatostatin has been reported to control upper gastrointestinal hemorrhage, prevent restraint stress-induced gastric ulcerations, and inhibit gastric acid secretion. In this study we examined the effect of somatostatin on basal and pentagastrin-stimulated gastric acid output and mucosal blood flow. Antral and corpus mucosal blood flows were measured by hydrogen gas clearance in fasted, anesthetized rats. Acid output was determined by a continuous gastric perfusion technique. In the basal study somatostatin in doses of 8, 16, and 32 micrograms . kg-1 . h-1 was infused intravenously in separate groups of animals. In the pentagastrin stimulation study somatostatin (16 micrograms . kg-1 . h-1) was infused after gastric acid output was stimulated to plateau by intravenous pentagastrin (19.8 micrograms . kg-1 . h-1). The results showed that somatostatin had no effect on basal corpus or antral mucosal blood flow. During pentagastrin stimulation somatostatin decreased acid secretion but increased corpus mucosal blood flow. We speculate that this increase in blood flow may not be a direct effect as basal corpus or antral mucosal blood flow was unaffected by somatostatin.

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Role of prostaglandins in regulation of gastric mucosal blood flow and acid secretion

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1992.263.4.g446 ◽

1992 ◽

Vol 263 (4) ◽

pp. G446-G451 ◽

Cited By ~ 3

Author(s):

L. Holm ◽

A. Jagare

Keyword(s):

Blood Flow ◽

Acid Secretion ◽

Acid Output ◽

Mucosal Blood Flow ◽

Gastric Mucosal Blood Flow ◽

Doppler Flowmetry ◽

Blood Flow Reduction ◽

Red Blood Cell Velocity ◽

Blood Flow Increase

The role of prostaglandins in the rat gastric mucosal vascular response to acid stimulation was studied. Blood flow was measured with laser-Doppler flowmetry (LDF) and with red blood cell velocity measurements in the superficial mucosa; acid secretion was determined by titration. Baseline acid output was calculated to be 0.026 +/- 0.011 mueq/min. Pentagastrin (20 and 40 micrograms.kg-1.h-1 iv) significantly increased acid output to 0.387 +/- 0.104 and 0.546 +/- 0.220 mueq/min and LDF to 119 +/- 10 and 132 +/- 13% of control, respectively. LDF was significantly reduced by 15% after indomethacin (3 mg/kg iv) and was not changed by pentagastrin, whereas acid secretion increased to similar levels as without indomethacin pretreatment. The H2-agonist impromidine (100 and 500 micrograms.kg-1.h-1 iv) induced a dose-dependent increase in acid secretion (0.178 +/- 0.068 and 0.330 +/- 0.072 mueq/min, respectively) while blood flow was unchanged. Despite a substantial blood flow reduction (-38%) by indomethacin, impromidine did not alter blood flow, and acid secretion was dose dependently increased to similar values as without indomethacin pretreatment. These results provide further evidence that there is not necessarily any correlation between blood flow and acid secretion and that the pentagastrin-induced blood flow increase depends on prostaglandin release.

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Renal failure increases gastric mucosal blood flow and acid secretion in rats: role of endothelium-derived nitric oxide

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1992.263.1.g75 ◽

1992 ◽

Vol 263 (1) ◽

pp. G75-G80 ◽

Cited By ~ 1

Author(s):

E. Quintero ◽

P. H. Guth

Keyword(s):

Nitric Oxide ◽

Renal Failure ◽

Blood Flow ◽

Chronic Renal Failure ◽

Acid Secretion ◽

Acid Output ◽

Muscle Blood Flow ◽

Specific Inhibitor ◽

Mucosal Blood Flow ◽

Gastric Mucosal Blood Flow

Because of the contradictory findings in clinical studies, and the complete lack of animal studies, the purpose of this investigation was to characterize the changes in gastric mucosal blood flow (GMBF) and acid secretion in an animal model of chronic renal failure. Rats with chronic renal failure induced by partial kidney infarction had a significantly higher basal GMBF and lower gastric vascular resistance than control rats. The gastric acid secretory and mucosal hyperemic response to pentagastrin were markedly enhanced in renal failure rats. Because endothelial-derived nitric oxide (NO) is an endogenous vasodilator that regulates gastric vascular tone, we hypothesized that NO mediates the gastric hyperemia of renal failure rats. The administration of N omega-nitro-L-arginine methyl ester (L-NAME), a specific inhibitor of NO formation, produced a significantly greater decrease in GMBF in renal failure rats than in control rats, including a low dose inhibiting the basal hyperemia in renal failure rats but having no effect in control rats. It also attenuated pentagastrin-stimulated GMBF in both groups. In contrast, L-NAME produced a similar decrease in basal skeletal muscle blood flow in both renal failure and control rats. We conclude that in the renal failure rat 1) there is an increased basal GMBF and pentagastrin-stimulated acid output and GMBF, and 2) this gastric mucosal hyperemia is mediated by NO.

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Blood flow limitation of stimulated gastric acid secretion in the rat

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1986.250.6.g794 ◽

1986 ◽

Vol 250 (6) ◽

pp. G794-G799

Author(s):

F. W. Leung ◽

G. L. Kauffman ◽

J. Washington ◽

O. U. Scremin ◽

P. H. Guth

Keyword(s):

Blood Flow ◽

Acid Secretion ◽

Gastric Acid Secretion ◽

Gastric Acid ◽

Acid Output ◽

Gastric Lavage ◽

Mucosal Blood Flow ◽

Hydrogen Gas ◽

Gastric Acid Output ◽

Gastric Corpus

Secretagogue-stimulated gastric acid output is reduced when gastric mucosal blood flow is below normal. We tested the hypothesis that the reduction in acid secretion associated with reduced mucosal blood flow was due to a decrease in the delivery of the secretagogue. Gastric acid output was determined by continuous gastric lavage with 0.15 M NaCl, and gastric corpus mucosal blood flow was measured by hydrogen gas clearance in anesthetized, pylorus-ligated rats before and during a period of hypovolemia-induced reduction in mucosal blood flow. A linear correlation between pentagastrin- and histamine-stimulated gastric acid output and gastric corpus mucosal blood flow during hypotension over a range of mucosal blood flow rates was found, and each was expressed as a percentage of the plateau values before hemorrhage. When the dose of pentagastrin was doubled or tripled, or when the stimulation of gastric acid secretion was vagus nerve stimulation, a stimulant of acid secretion that is independent of blood flow for secretatogue delivery, the reduction in gastric acid output by hypotension was not reversed. We conclude that stimulated gastric acid secretion during hemorrhagic hypotension is blood flow-limited and not related to inadequate delivery of secretagogue to parietal cells.

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