Strong gastric contractions cause mucosal ischemia

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.

Download Full-text

Vagal nerve stimulation causes noncholinergic dilatation of gastric arterioles

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1986.250.5.g660 ◽

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.

Download Full-text

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.

Download Full-text

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

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1996.271.6.g1028 ◽

1996 ◽

Vol 271 (6) ◽

pp. G1028-G1033 ◽

Cited By ~ 2

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.

Download Full-text

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

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1997.272.6.g1473 ◽

1997 ◽

Vol 272 (6) ◽

pp. G1473-G1480 ◽

Cited By ~ 11

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.

Download Full-text

Platelet Adhesion in Polytetrafluoroethylene (PTFE) Vascular Grafts In Vivo and the Influence of Increased Intramuscular Pressure-An Experimental Model

Thrombosis and Haemostasis ◽

10.1055/s-0038-1665334 ◽

1983 ◽

Vol 50 (04) ◽

pp. 881-884 ◽

Cited By ~ 3

Author(s):

J T Christenson ◽

P Qvarfordt ◽

S-E Strand ◽

D Arvidsson ◽

T Sjöberg ◽

...

Keyword(s):

Blood Flow ◽

Graft Failure ◽

Small Diameter ◽

Graft Material ◽

Intramuscular Pressure ◽

Initial Flow ◽

Early Graft ◽

Wick Technique ◽

Early Graft Failure

SummaryThrombogenicity of graft material is involved in early graft failure in small diameter grafts. The frequently seen postoperative swelling of the leg after distal revascularization may cause an increased intramuscular pressure and early graft failure.Pairs of 4 mm polytetrafluoroethylene (PTFE) grafts were implanted. Autologous platelets were labeled with mIn-oxine. Platelet adhesiveness onto the grafts were analyzed from gamma camera images. Intramuscular pressures were measured with wick technique. Blood flow was measured. One graft served as control the other as test graft. Ninety minutes after declamping the i. m. pressure was increased in the test-leg to 30 mmHg, and later to 60 mmHg.In the control-graft platelet uptake increased to a maximum 60 min after declamping. Blood flow and i.m. pressure remained uneffected. The test-grafts were initially similar but when i.m. pressure was increased to 30 mmHg activity in the grafts increased significantly. Blood flow decreased with 12% of initial flow. When i. m. pressure was raised to 60 mmHg platelet uptake continued to increase.An increased intramuscular pressure of 30 mmHg or more significantly increase the amount of platelets adhering onto PTFE grafts, emphasizing the need for measuring intramuscular pressures after lower limb vascular revascularizations.

Download Full-text

Preclinical Quantification of Prostate Cancer-Associated Vascular Alterations in the Bone Microenvironment in vivo

European Surgical Research ◽

10.1159/000514224 ◽

2020 ◽

Vol 61 (6) ◽

pp. 188-200

Author(s):

Malte Schroeder ◽

Lennart Viezens ◽

Jördis Sündermann ◽

Svenja Hettenhausen ◽

Gerrit Hauenherm ◽

...

Keyword(s):

Prostate Cancer ◽

Blood Flow ◽

Flow Velocity ◽

Cell Lines ◽

Blood Flow Velocity ◽

Tumour Growth ◽

Prostate Cancer Cell ◽

Bone Microenvironment ◽

Prostate Cancer Cell Lines

Introduction: Prostate cancer has a special predilection to form bone metastases. Despite the known impact of the microvascular network on tumour growth and its dependence on the organ-specific microenvironment, the characteristics of the tumour vasculature in bone remain unknown. Methods: The cell lines LNCaP, DU145, and PC3 were implanted into the femurs of NSG mice to examine the microvascular properties of prostate cancer in bone. Tumour growth and the functional and morphological alterations of the microvasculature were analysed for 21 days in vivo using a transparent bone chamber and fluorescence microscopy. Results: Vascular density was significantly lower in tumour-bearing bone than in non-tumour-bearing bone, with a marked loss of small vessels. Accelerated blood flow velocity led to increased volumetric blood flow per vessel, but overall perfusion was not affected. All of the prostate cancer cell lines had similar vascular patterns, with more pronounced alterations in rapidly growing tumours. Despite minor differences between the prostate cancer cell lines associated with individual growth behaviours, the same overall pattern was observed and showed strong similarity to that of tumours growing in soft tissue. Discussion: The increase in blood flow velocity could be a specific characteristic of prostate cancer or the bone microenvironment.

Download Full-text

An autoradiographic study of regional distribution of gastric mucosal blood flow

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1988.254.4.g566 ◽

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.

Download Full-text