Adenosine A2-receptor mediates ethanol-induced arteriolar dilation in rat stomach

1996 ◽  
Vol 271 (6) ◽  
pp. G1028-G1033 ◽  
Author(s):  
H. Nagata ◽  
E. Sekizuka ◽  
T. Morishita ◽  
M. Tatemichi ◽  
T. Kurokawa ◽  
...  
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Human Calcitonin ◽  
Rat Stomach ◽  
Microscopy Technique ◽  
Vasoactive Substances ◽  
Adenosine A2 Receptor

Topical application of ethanol to the gastrointestinal mucosa induces vasodilation. Using an in vivo microscopy technique, we studied the effect of topical ethanol on the submucosal microvessels that control mucosal blood flow in the rat stomach and identified vasoactive substances and receptors that mediate the ethanol vasoaction. Topical ethanol (1-20%) dilated submucosal arterioles dose dependently, but did not change venular diameters. An inhibitor of alcohol dehydrogenase, 1 mM 4-methylpyrazole, did not alter the ethanol vasoaction. Ethanol-induced arteriolar dilation was eliminated by adenosine deaminase, but other vasodilator inhibitors such as atropine, pyrilamine, indomethacin, human calcitonin gene-related peptide-(8-37), and N omega-nitro-L-arginine methyl ester did not prevent it. Ethanol-induced arteriolar dilation was inhibited by an adenosine A2-receptor antagonist, but not by an A1-receptor antagonist, whereas an A2-agonist, but not an A1-agonist, dose dependently dilated arterioles. Exogenous adenosine (10(-5)-10(-3) M) dilated arterioles to a similar extent as ethanol. This response was inhibited by an A2-antagonist. We conclude that nonmetabolized ethanol increases gastric mucosal blood flow via A2-receptors in submucosal arterioles.

Vagal nerve stimulation causes noncholinergic dilatation of gastric arterioles

1986 ◽  
Vol 250 (5) ◽  
pp. G660-G664
Author(s):  
T. Morishita ◽  
P. H. Guth
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
In Vivo Microscopy ◽  
Vasodilator Effect ◽  
Splitting Technique

Vagal nerve stimulation causes prompt dilatation of gastric submucosal arterioles (the vessels that control gastric mucosal blood flow) in rats. In vivo microscopy was used to determine whether this direct vasodilator effect of vagal nerve stimulation on rat gastric submucosal arterioles is mediated by cholinergic fibers. Acetylcholine and atropine were topically applied to the submucosa. The distal end of the severed vagus nerve was electrically stimulated (8 V, 2 ms, 6 Hz, 20 s) subdiaphragmatically. Diameter changes of the submucosal arterioles were videotaped and measured with an image-splitting technique on playback of the videotapes. Acetylcholine, 10(-7) to 10(-5) M, dilated the arterioles dose dependently. Atropine prevented the acetylcholine-induced dilatation, 10(-5) M, nearly completely inhibiting the dilatation. Vagal nerve stimulation dilated the arterioles promptly, and this dilatation was not blocked by 10(-5) M atropine, a dose that blocked the acetylcholine-induced dilatation. These results indicate that vagal nerve stimulation causes atropine-resistant, noncholinergic dilatation of gastric submucosal arterioles in rats.

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

1994 ◽  
Vol 267 (1) ◽  
pp. G94-G104 ◽  
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.

Circadian rhythm in gastric mucosal blood flow in fasting rat stomach

1991 ◽  
Vol 51 (4) ◽  
pp. 275-280 ◽  
Author(s):  
Kenneth R. Larsen ◽  
Merril T. Dayton ◽  
John G. Moore
Keyword(s):  
Blood Flow ◽  
Circadian Rhythm ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Rat Stomach

Human spasmolytic polypeptide decreases proton permeation through gastric mucus in vivo and in vitro

1997 ◽  
Vol 272 (6) ◽  
pp. G1473-G1480 ◽  
Author(s):  
S. Tanaka ◽  
D. K. Podolsky ◽  
E. Engel ◽  
P. H. Guth ◽  
J. D. Kaunitz
Keyword(s):  
Blood Flow ◽  
Intracellular Ph ◽  
Ussing Chamber ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Gastric Mucus ◽  
Doppler Flowmetry ◽  
Mucus Gel

Exogenously administered trefoil peptides are gastroprotective in rat injury models. We hypothesized that trefoil-associated gastroprotection occurred by decreasing the rate of proton permeation through mucus. Gastric surface cell intracellular pH and mucus gel thickness were measured by in vivo microscopy. Gastric mucosal blood flow was measured by laser-Doppler flowmetry. The effect of human spasmolytic peptide (hSP) on H+ diffusion through 5% purified porcine mucin was measured using an Ussing chamber. Buffering action of mucin was measured by titration. In vivo, gastric mucosal blood flow and mucus gel thickness were not affected by any of the treatments. Topical hSP, but not intravenous hSP, decreased initial acidification rate and elevated the intracellular pH of gastric surface cells during luminal acid challenge. In in vitro studies, hSP dose dependently decreased the diffusion coefficient of H+ through 5% porcine mucin solution. hSP had no significant effect on the buffering action of mucin solutions. These data support our hypothesis that hSP interacts with gastric mucin in a manner that inhibits proton permeation through the mucus gel layer.

Effect of a leukotriene receptor antagonist on LTC4 vasoconstriction in rat stomach

1990 ◽  
Vol 259 (1) ◽  
pp. G147-G154
Author(s):  
Y. Yonei ◽  
P. H. Guth
Keyword(s):  
Receptor Antagonist ◽  
In Vivo Microscopy ◽  
Leukotriene Receptor Antagonist ◽  
Rat Stomach ◽  
Cysteinyl Leukotriene ◽  
Microscopy Technique ◽  
Plot Analysis ◽  
Microvascular Response ◽  
Leukotriene Receptor

With the use of an in vivo microscopy technique in anesthetized-laparotomized rats, the effect of L660,711, a cysteinyl-leukotriene (LT) receptor antagonist, on the gastric submucosal microvascular response to leukotrienes was studied. The direct application of 50-400 nM LTC4 onto the exposed submucosal vasculature caused constriction of both arterioles (maximum constriction: 24 +/- 3%) and venules (26 +/- 3%), whereas LTD4 had no significant effect. Pretreatment with 5 mg/kg L660,711 intragastrically significantly attenuated the LTC4-induced vasoconstriction. The submucosal application of 2 x 10(-7) to 2 x 10(-2) M L660,711 dose dependently inhibited the 400 nM LTC4-induced vasoconstriction. The IC50 of L660,711, preapplied to the gastric submucosa for 15 min, was 4.4 x 10(-4) M in arterioles and 3.9 x 10(-4) M in venules, and 3.6 x 10(-5) M and 3.2 x 10(-5) M, respectively, when it was applied simultaneously with LTC4. Schild plot analysis revealed that L660,711 was not a pure competitive receptor antagonist. L660,711 had no significant effects on epinephrine- or vasopressin-induced arteriolar constriction. In conclusion, L660,711 significantly antagonizes the gastric microvascular effects of LTC4, but not those of other vasoconstrictors, and appears to be a useful new tool for studying LTC4 effects.

Strong gastric contractions cause mucosal ischemia

1991 ◽  
Vol 260 (3) ◽  
pp. G524-G530 ◽  
Author(s):  
E. H. Livingston ◽  
T. J. Howard ◽  
T. R. Garrick ◽  
E. P. Passaro ◽  
P. H. Guth
Keyword(s):  
Blood Flow ◽  
Flow Velocity ◽  
Capillary Flow ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Initial Flow ◽  
Force Transducers ◽  
Gastric Contractions ◽  
Muscularis Externa

Contractions of a segment of bowel result in alterations of its blood flow. However, the precise temporal and spacial relationships between contractions and mucosal blood flow are unknown. Rats were fitted with strain gauge force transducers and implanted with silver wire electrodes into the muscularis externa of the stomach. In vivo microscopic observation of motility and of the gastric mucosal blood flow was performed during electrical field-stimulated contractions. Contractions originated in the midcorpus, were 0.237 +/- 0.018 cm wide, traveled along the corpus at 0.133 +/- 0.024 cm/s, and had a duration of 5.9 +/- 0.1 s. Antral contractions were 0.174 +/- 0.032 cm wide, traveled at 0.070 +/- 0.009 cm/s, and had a duration of 5.6 +/- 0.7 s. During the contraction, capillary flow velocity in the corpus decreased from a basal value of 410 +/- 105 to 206 +/- 104 microns/s at the peak of a contraction. Five seconds after the contraction was released hyperemia was observed with the flow velocity increasing to 570 +/- 102 microns/s. In the antrum, flow stopped completely during the contraction irrespective of the initial flow velocity and no hyperemia occurred with release of the contraction; rather, flow velocity slowly returned to baseline values. In both regions the flow reductions were in phase with the contractions as measured by the force transducers. These studies provide direct evidence that strong gastric contractions can effectively reduce or stop gastric mucosal blood flow.

An autoradiographic study of regional distribution of gastric mucosal blood flow

1988 ◽  
Vol 254 (4) ◽  
pp. G566-G574
Author(s):  
W. J. Angerson ◽  
J. G. Geraghty ◽  
D. C. Carter
Keyword(s):  
Blood Flow ◽  
Regional Distribution ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Autoradiographic Study ◽  
Acute Injury ◽  
Antral Mucosa ◽  
Blood Flows ◽  
Greater Curvature ◽  
Mucosal Folds

Iodo[14C]antipyrine autoradiography was used to measure gastric mucosal blood flow in anesthetized rats and to study regional distribution. Blood flows of 61 +/- 8 ml.100 g-1.min-1 (means +/- SE) in corpus and 84 +/- 9 ml.100 g-1.min-1 in antral mucosa compared well with previously reported measurements by hydrogen clearance. Blood flow in the crests of corpus mucosal folds was significantly higher than in the valleys between folds, indicating that the greater susceptibility of the former areas to acute injury, documented in several studies, is not associated with a perfusion defect in the resting stomach. Corpus mucosal blood flow was also higher in the side walls of the stomach than in the greater curvature region, and in distal than in proximal locations. No systematic regional variations within antral mucosa were demonstrated.

Gastric Mucosal Blood Flow Before and After TAE

1991 ◽  
Vol 3 (4) ◽  
pp. 513-518 ◽  
Author(s):  
Tadatoshi TSUCHIGAME ◽  
Kohshiro ITOH ◽  
Masafumi HAR ◽  
Okimitsu WATANABE ◽  
Youichi OHYAMA ◽  
...  
Keyword(s):  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Before And After
Sign in / Sign up

Export Citation Format

Share Document