Histamine is involved in gastric vasodilation during acid back diffusion via activation of sensory neurons

2002 ◽  
Vol 283 (3) ◽  
pp. G603-G611 ◽  
Author(s):  
Astrid Rydning ◽  
Oddveig Lyng ◽  
Sture Falkmer ◽  
Jon Erik Grønbech
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Sensory Neurons ◽  
Cell Mass ◽  
Ruthenium Red ◽  
Sensory Nerves ◽  
Back Diffusion ◽  
Mediator Systems ◽  
Rat Gastric Mucosa ◽  
And Control

Protective vasodilation during acid back diffusion into the rat gastric mucosa depends on activation of sensory neurons and mast cell degranulation with histamine release. We hypothesized that these two mediator systems interact and that histamine partly exerts its effect via sensory nerves. Gastric blood flow (GBF) and luminal histamine were measured in chambered stomachs, and mast cell numbers were assessed by morphometry. Ablation of sensory neurons and depletion of mast cells were produced by pretreatment with capsaicin or dexamethasone, respectively. Mucosal exposure to 1.5 M NaCl and then to pH 1.0 saline in ablated and control rats caused increased luminal histamine and reduced numbers of mast cells. Enterochromaffin-like cell marker pancreastatin remained unchanged. Only control rats responded with an increase in GBF. Capsaicin stimulation (640 μM) of the undamaged mucosa induced identical increase in GBF and unchanged mast cell mass in normal and dexamethasone-treated rats. Increase in GBF after topical exposure to histamine (30 mM) in rats pretreated with capsaicin or a calcitonin gene-related peptide (CGRP)1antagonist human CGRP8–37or exposed to the calcium pore blocker ruthenium red was less than one-half of that in control rats. These data suggest that mast cell-derived histamine is involved in gastric vasodilatation during acid back diffusion partly via sensory neurons.

Mast cell-nerve fiber interaction: Ultrastructural studies

1990 ◽  
Vol 48 (3) ◽  
pp. 428-429
Author(s):  
E.Y. Chi ◽  
M.L. Su ◽  
Y.T. Tien ◽  
W.R. Henderson
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Substance P ◽  
Nerve Fiber ◽  
Sensory Nerves ◽  
Ultrastructural Studies ◽  
Morphological Studies ◽  
Granulocyte Infiltration ◽  
Intracutaneous Injection ◽  
Recent Attention

Recent attention has been directed to the interaction of the nerve and immune systems. The neuropeptide substance P, a tachykinnin which is a neurotransmitter in the central and peripheral nervous systems produces tissue swelling, augemntation of intersitial fibrin deposition and leukocyte infiltration after intracutaneous injection. There is a direct correlation reported between the extent of mast cell degranulation at the sites of injection and the tissue swelling or granulocyte infiltration. It has previously been demonstrated that antidromic electrical stimulation of sensory nerves induces degranulation of cutaneous mast cells, cutaneous vasodilation and augmented vascular permeability. Morphological studies have documented a close anatiomical association between mast cells and nonmyelinated nerves, that contain substance P and other neuropeptides. However, the presence of mast cells within nerve fasicles has not been previously examined ultrastructurally. In this study, we examined ultrastructurally the distribution of mast cells in the nerve fiber bundles located in the muscular connective tissue of rat tongues (n=20).

Phenotypic and Quantitative Changes in Mast Cells after Syngeneic Unilateral Lung Transplantation in the Rat

1996 ◽  
Vol 91 (3) ◽  
pp. 319-327 ◽  
Author(s):  
Annick Buvry ◽  
Monique Garbarg ◽  
Violetta Dimitriadou ◽  
Agnès Rouleau ◽  
George F. J. Newlands ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Lung Transplantation ◽  
Left Lung ◽  
Muscle Layer ◽  
Rat Lung ◽  
Large Airways ◽  
Quantitative Changes ◽  
Cell Phenotypes ◽  
And Control

1. Lung transplantation causes a total interruption of the innervation and vascularization within the transplanted organ, followed by repair processes. This is frequently associated with bronchial hyper-responsiveness. A common feature of tissue repair is an increase in the number of mast cells. Three phenotypically distinct mast cell subsets, with respect to their protease content, have been identified in rat lung, and it is probable that mast cells of differing protease phenotype fulfil different functions. 2. We have compared the number, protease phenotype and distribution of mast cells in left lung from transplanted and control Lewis rats 1 month after syngeneic unilateral left lung transplantation, without interference of inflammation, graft rejection or of any treatment. Connective and mucosal-type mast cell phenotypes were characterized using antibodies directed against their specific rat mast cell proteases, RMCPI and RMCPII, respectively. 3. After transplantation, RMCPI and RMCPII tissue concentrations increased by 172% and 239%, respectively, compared with controls (13.1 ± 1.2 and 5.6±1.0 μg/g). 4. Localization of mast cell phenotypes was studied by immunohistochemistry after double immunostaining. The number of mast cells increased after transplantation: the increase in the number of RMCPI-immunoreactive mast cells (RMCPI+) was significant around bronchioles and arterioles, around large vessels and in the pleura. The number of RMCPII+ mast cells also significantly increased around bronchioles and arterioles, as well as in the smooth muscle layer of large airways. Some mast cells stained for the presence of both RMCPI and RMCPII, supporting the existence of co-expressing phenotype in rat lung. The number of mast cells of the RMCPI+ /H+ phenotype significantly increased around bronchioles and arterioles and in the pleura. Moreover, the distribution of the mast cell phenotypes was modified in the different areas after transplantation. 5. This indicates a local differentiation/maturation of mast cells after transplantation.

Mast cells are involved in the gastric hyperemic response to acid back diffusion via release of histamine

2001 ◽  
Vol 280 (6) ◽  
pp. G1061-G1069 ◽  
Author(s):  
Astrid Rydning ◽  
Oddveig Lyng ◽  
Birgitte Lid Adamsen ◽  
Sture Falkmer ◽  
Arne K. Sandvik ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Chromogranin A ◽  
Ex Vivo ◽  
Back Diffusion ◽  
Rat Stomach ◽  
Stomach Mucosa ◽  
Mucosal Mast Cells ◽  
Receptor Blockers ◽  
Hyperemic Response

Acid back diffusion into the rat stomach mucosa leads to gastric vasodilation. We hypothesized that histamine, if released from the rat mucosa under such conditions, is mast cell derived and involved in the vasodilator response. Gastric blood flow (GBF) and luminal histamine were measured in an ex vivo chamber. Venous histamine was measured from totally isolated stomachs. Mucosal mast cells (MMC), submucosal connective tissue mast cells (CTMC), and chromogranin A-immunoreactive cells (CgA IR) were assessed morphometrically. After mucosal exposure to 1.5 M NaCl, the mucosa was subjected to saline at pH 5.5 (control) or pH 1.0 (H+back diffusion) for 60 min. H+back diffusion evoked a marked gastric hyperemia, increase of luminal and venous histamine, and decreased numbers of MMC and CTMC. CgA IR cells were not influenced. Depletion of mast cells with dexamethasone abolished (and stabilization of mast cells with ketotifen attenuated) both hyperemia and histamine release in response to H+back diffusion. GBF responses to H+back diffusion were attenuated by H1and abolished by H3but not H2receptor blockers. Our data conform to the idea that mast cells are involved in the gastric hyperemic response to acid back diffusion via release of histamine.

scholarly journals Mast Cell Degranulation and Adenosine Release:Acupoint Specificity for Effect of Electroacupuncture on Pituitrin-Induced Acute Heart Bradycardia in Rabbits

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Xuezhi Wang ◽  
Meng Huang ◽  
Hongwei Yang ◽  
Di Zhang ◽  
Wei Yao ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mast Cell ◽  
Mast Cells ◽  
Mast Cell Degranulation ◽  
Control Points ◽  
Model Group ◽  
Adenosine Release ◽  
Specificity Of Acupoints ◽  
Acupoint Specificity ◽  
And Control

Acupuncture is a medical modality based on the theory of traditional Chinese medicine, and its effect is relatively dependent on acupoint specificity. However, there is little knowledge on acupoint specificity versus acupuncture outcomes because of the deficiency of rigorous investigation on this topic, which has impeded the growing legitimacy of acupuncture in the mainstream of medicine as an evidence-based therapy. Therefore, it is of utmost importance to clarify this critical issue. The present study aims to verify the phenomenon of acupoint specificity in acupuncture-induced cardiovascular regulation and explore the biological mechanism by measuring mast cells’ degranulation and adenosine release. This study was conducted to explore the specificity of acupoints in an acute bradycardia rabbit model. After electroacupuncture (EA) stimulation at PC6, PC control (con) 1, PC con 2, LU7, LI11, and nonacupoint, only the PC6 group showed a significant improvement in relative heart rate as compared to that of the model group. There was no significant difference between the relative heart rate of other EA groups and that of the model group. Historical results also showed that the ratio of degranulated mast cells in PC6 was significantly higher than other acupoints and control points. From the results of high-performance liquid chromatography (HPLC), a transient elevation of adenosine concentration during EA was only observed on acupoints and control points ( P < 0.05 ) along the pericardium meridian. The EA-induced adjustment on acute bradycardia exhibits a relative specificity of acupoints, which may be related to mast cell degranulation and adenosine release in local acupoint areas. Increased degranulation of mast cells and augmentation of adenosine release during EA may be the mechanisms for PC6 having significantly better acupuncture effects than other acupoints and nonacupoints.

scholarly journals Neuro-immune interactions in chemical-induced airway hyperreactivity

2016 ◽  
Vol 48 (2) ◽  
pp. 380-392 ◽  
Author(s):  
Fien C. Devos ◽  
Brett Boonen ◽  
Yeranddy A. Alpizar ◽  
Tania Maes ◽  
Valérie Hox ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Transient Receptor Potential ◽  
Chinese Hamster ◽  
Transient Receptor Potential Channels ◽  
Airway Hyperreactivity ◽  
Sensory Nerves ◽  
Wild Type ◽  
Immunological Parameters

Asthma may be induced by chemical sensitisers,viamechanisms that are still poorly understood. This type of asthma is characterised by airway hyperreactivity (AHR) and little airway inflammation. Since potent chemical sensitisers, such as toluene-2,4-diisocyanate (TDI), are also sensory irritants, it is suggested that chemical-induced asthma relies on neuro-immune mechanisms.We investigated the involvement of transient receptor potential channels (TRP) A1 and V1, major chemosensors in the airways, and mast cells, known for their ability to communicate with sensory nerves, in chemical-induced AHR.In vitrointracellular calcium imaging and patch-clamp recordings in TRPA1- and TRPV1-expressing Chinese hamster ovarian cells showed that TDI activates murine TRPA1, but not TRPV1. Using anin vivomodel, in which an airway challenge with TDI induces AHR in TDI-sensitised C57Bl/6 mice, we demonstrated that AHR does not develop, despite successful sensitisation, inTrpa1andTrpv1knockout mice, and wild-type mice pretreated with a TRPA1 blocker or a substance P receptor antagonist. TDI-induced AHR was also abolished in mast cell deficientKitWsh/Wshmice, and in wild-type mice pretreated with the mast cell stabiliser ketotifen, without changes in immunological parameters.These data demonstrate that TRPA1, TRPV1 and mast cells play an indispensable role in the development of TDI-elicited AHR.

scholarly journals Abnormal mast cell granules in the beige (Chédiak-Higashi syndrome) mouse.

1975 ◽  
Vol 23 (2) ◽  
pp. 117-122 ◽  
Author(s):  
E Y Chi ◽  
D Lagunoff
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Alcian Blue ◽  
Toluidine Blue ◽  
Ruthenium Red ◽  
Chediak Higashi Syndrome

Mast cells of beige (C57BL/6J) (bg-j/bg-j) mice were examined histochemically and ultrastructurally. Mast cell granules in the beige mice were markedly enlarged and irregular in shape. Granule contents stained uniformly with acidified toluidine blue, but with ruthenium red and Alcian Blue-safranin, two components were evident. The rims of the abnormal granules stained with ruthenium red and with Alcian Blue; the centers of the granules were clear with ruthenium red and stained with safranin. Mast cell granules thus represent another abnormal organelle in the Chédiak-Higashi syndrome.

Capsaicin-induced hyperemia in the stomach: possible contribution of mast cells

1992 ◽  
Vol 263 (2) ◽  
pp. G209-G214 ◽  
Author(s):  
J. L. Wallace ◽  
G. W. McKnight ◽  
A. D. Befus
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Gastric Mucosa ◽  
Ruthenium Red ◽  
Nippostrongylus Brasiliensis ◽  
Afferent Neurons ◽  
Topical Capsaicin ◽  
H1 Receptor Antagonist ◽  
Prior Infection ◽  
Hyperemic Response

Topical application of capsaicin to the gastric mucosa results in marked hyperemia as a consequence of the release of vasoactive neuropeptides from sensory afferent neurons. Because many of these neuropeptides have the capacity to induce mast cell degranulation, we investigated the possible contribution of mast cells to capsaicin-induced hyperemia. Application of capsaicin to the gastric mucosa of normal rats resulted in a concentration-dependent increase in blood flow. In rats in which mastocytosis was induced by prior infection with Nippostrongylus brasiliensis, the hyperemic responses to capsaicin were significantly greater than in control rats. This augmented hyperemic response could be significantly attenuated by pretreatment with a histamine H1-receptor antagonist (pyrilamine) or with a mast cell stabilizer (doxantrazole). Depletion of mucosal mast cells through treatment with dexamethasone also significantly reduced the hyperemic response to capsaicin. Hyperemic response to capsaicin in normal rats and in rats with mucosal mastocytosis could be completely abolished by pretreatment with ruthenium red or prior ablation of the sensory afferent neurons with capsaicin. These results suggest that in rats with gastric mastocytosis, sensory neuron-dependent activation of mast cells contributes to the hyperemic response to topical capsaicin. These findings are therefore consistent with the hypothesis that there is communication between nerves and mast cells in the gastric mucosa, at least in rats previously infected with N. brasiliensis.

Substance P may attenuate gastric hyperemia by a mast cell-dependent mechanism in the damaged gastric mucosa

1999 ◽  
Vol 277 (5) ◽  
pp. G1064-G1073 ◽  
Author(s):  
Astrid Rydning ◽  
Oddveig Lyng ◽  
Steinar Aase ◽  
Jon Erik Grønbech
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Substance P ◽  
Gastric Mucosa ◽  
Sensory Neurons ◽  
Laser Doppler Flow ◽  
Calcitonin Gene ◽  
Acid Challenge ◽  
Dependent Mechanism

Calcitonin gene-related peptide (CGRP) released from sensory neurons, which are closely apposed to mast cells and blood vessels, mediates gastric hyperemia in response to acid challenge of the damaged mucosa. Substance P (SP) is coreleased with CGRP from sensory neurons, but the role of this peptide in gastric blood flow regulation is largely unknown. Chambered rat stomachs were exposed to 1.5 M NaCl and acidic saline after treatment with SP, aprotinin (serine protease inhibitor), and the mast cell stabilizers ketotifen and sodium cromoglycate (SCG). Gastric hyperemia (measured with a laser Doppler flow velocimeter) after hypertonic injury and acid challenge was nearly abolished by SP. Aprotinin infused together with SP and pretreatment with ketotifen and SCG before SP restored the gastric hyperemia. Ketotifen and SCG inhibited mast cell degranulation in SP-treated rats. Preservation of gastric hyperemia was correlated with improved mucosal repair. These data suggest that impaired hyperemia by SP during acid challenge of the gastric mucosa may be mediated by a mast cell-dependent mechanism involving the release of proteases from mast cells.

Inosine-induced vasoconstriction is mediated by histamine and thromboxane derived from mast cells

1996 ◽  
Vol 270 (2) ◽  
pp. H560-H566 ◽  
Author(s):  
R. K. Shepherd ◽  
B. R. Duling
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Ruthenium Red ◽  
Mast Cell Degranulation ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Cell Staining ◽  
Subsequent Response ◽  
Cheek Pouches

Mast cell degranulation has been shown to release products that cause arteriolar constriction. We previously reported that two nucleosides, adenosine and inosine, cause vasoconstriction of isolated hamster cheek pouch arterioles by stimulating degranulation of periarteriolar mast cells. The objectives of the present study were to characterize the nucleoside-dependent vasoconstriction in vivo and to determine the mediator or mediators responsible. We examined the vasomotor effect of inosine on arterioles in the cheek pouches of anesthetized hamsters (70 mg/kg pentobarbital sodium) in the control situation and in the presence of receptor antagonists for histamine (H1), thromboxane A2 (Tx), and leukotrienes (LT). Most experiments were carried out using inosine applied once locally via micropipette to arterioles and observing the subsequent response. Over a range of inosine concentrations from 10(-5) to 10(-3) M in the pipette, we observed a dose-dependent increase in the incidence and magnitude of constriction. In addition, mast cell staining with ruthenium red was observed after stimulation with inosine, an indication of mast cell degranulation. Neither the H1, Tx, nor LT antagonist alone had a significant effect on the vasomotor response to inosine. However, combined H1 and Tx blockade significantly reduced the incidence and magnitude of inosine-induced constriction. These data establish that inosine-induced constriction occurs in vivo and support the role of mast cells in this response. Furthermore they suggest that multiple mediators, primarily histamine and thromboxane, are responsible for the observed constriction.

EFFECTS OF DEXAMETHASONE, PREDNISOLONE AND CORTISOL ON THE MAST CELLS AND TISSUE EOSINOPHILS IN RAT GASTRIC MUCOSA

1962 ◽  
Vol 41 (3) ◽  
pp. 432-436 ◽  
Author(s):  
Toimi Räsänen
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Mast Cell Degranulation ◽  
The Body ◽  
Water Soluble ◽  
Soluble Form ◽  
Tissue Eosinophilia ◽  
Mucosal Mast Cells ◽  
Rat Gastric Mucosa ◽  
Intact Rats

ABSTRACT Intact rats were injected intramuscularly at 8-hourly intervals with equal amounts, 6×1.0 mg, of dexamethasone (16α-methyl-9α-fluoro-prednisolone) as phosphate, prednisolone (11β,17,21-trihydroxy-pregna-1,4-diene-3,20-dione) and cortisol (11β,17,21-trihydroxy-pregn-4-ene-3,20-dione) both as succinates, all three in water soluble form. The rats were decapitated 4 hours after the last injection and the mucosal mast cells and tissue eosinophilic cells in the body mucosa of the glandular stomach counted. Calculation of the mast cell degranulation and the destruction of tissue eosinophils during the experiment gave the following degranulation coefficients for the degranulation of gastric mucosal mast cells: 0.541 for dexamethasone, 0.177 for prednisolone and 0.088 for cortisol. The corresponding destruction coefficients for the loss of tissue eosinophilia were 0.858, 0.156 and 0.124. It is suggested that the degranulation and destruction coefficients obtained in the investigation are correlated with the catabolic biological activity of the glucocorticoids.

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