Effect of histamine on microvascular permeability in the rat stomach

1983 ◽  
Vol 245 (2) ◽  
pp. G201-G207
Author(s):  
H. Nagata ◽  
P. H. Guth
Keyword(s):  
Histamine Receptors ◽  
Microvascular Permeability ◽  
In Vivo Microscopy ◽  
Rat Stomach ◽  
Serosal Surface ◽  
H2 Antagonist ◽  
H1 Antagonist ◽  
Dose Dependent ◽  
Muscularis Externa

The effect of histamine on gastric microvascular permeability to macromolecules in the rat was studied using fluorescent in vivo microscopy. Histamine was applied topically to the serosal surface for study of the muscularis externa, to the submucosa, and to the superficial mucosa, and the area of leaks of a fluorescein-albumin conjugate from microvessels was quantitated. In the muscularis externa both histamine and an H1-agonist, but not an H2-agonist, caused dose-dependent leak of conjugate from venules. An H1-antagonist, but not an H2-antagonist, decreased the histamine-induced leak. In the submucosa histamine caused dose-dependent dilatation of arterioles but not leak of conjugate. In contrast, bradykinin caused both dose-dependent dilatation of arterioles and leak of conjugate from venules. In the superficial mucosa histamine did not cause any leak. In conclusion, topical histamine 1) increased microvascular permeability to macromolecules from venules in the muscularis externa via H1-receptors, 2) did not affect microvascular permeability in the submucosa (this may be due to lack of histamine receptors on the venules as bradykinin increased venular permeability), and 3) did not affect microvascular permeability in the superficial mucosa, but there might not have been adequate histamine backdiffusion.

Distribution of histamine receptors in isolated canine airways

1983 ◽  
Vol 54 (3) ◽  
pp. 693-700 ◽  
Author(s):  
S. L. Bradley ◽  
J. A. Russell
Keyword(s):  
Smooth Muscle ◽  
Histamine Receptors ◽  
Receptor Activity ◽  
Histamine H2 Receptor ◽  
H2 Receptor ◽  
H2 Antagonist ◽  
Histamine H1 Receptors ◽  
H1 Antagonist ◽  
Dose Dependent

The distribution of histamine receptors was examined in isolated trachealis smooth muscle strips and helical strips of large (5 mm) and small (1.5 mm) intrapulmonary airways. All airways contracted in response to histamine, but the sensitivity to this agent was significantly greater in intrapulmonary airways than in trachealis strips. A dose-dependent tachyphylaxis to histamine occurred when airways were exposed repeatedly to 10(-4) M histamine but not to 5 X 10(-6) M histamine. The H1-agonist, 2-methylhistamine, also caused airway contractions, although they were less forceful than those caused by histamine. Both histamine- and 2-methylhistamine-induced contractions were blocked by the H1-antagonist, pyrilamine. The H2-agonists, 4-methylhistamine and dimaprit, as well as histamine in the presence of pyrilamine failed to relax both acetylcholine- and 5-hydroxytryptamine-induced contractions. Moreover, the H2-antagonist, metiamide, had no effect on histamine-induced contractions. We conclude that histamine H1-receptors are present in both extrapulmonary and intrapulmonary airways of the dog and cause contraction when stimulated. In contrast, histamine H2-receptor activity could not be demonstrated in the airways of this species.

Biochemical and physiological effects of compound 48/80 on canine trachea in vivo

1983 ◽  
Vol 54 (3) ◽  
pp. 720-729 ◽  
Author(s):  
A. R. Leff ◽  
J. K. Brown ◽  
M. Frey ◽  
B. Reed ◽  
W. M. Gold
Keyword(s):  
Mast Cells ◽  
Muscle Tension ◽  
Arterial Blood ◽  
Marked Variability ◽  
H2 Antagonist ◽  
Anesthetized Dogs ◽  
Threshold Doses ◽  
Tracheal Tissue ◽  
H1 Antagonist

We studied changes in tracheal histamine content and tracheal muscle tension after degranulation of tracheal mast cells by compound 48/80 in 32 anesthetized dogs. In four dogs compound 48/80 caused an increase in tracheal tension [13 +/- 5 (SD) g/cm], while femoral arterial blood pressure decreased only 14 +/- 11%. Tracheal tissue histamine decreased 17 +/- 6% in five dogs receiving intra-arterial compound 48/80 (5 X 10(-3) to 10(-1) mg/kg). Chlorpheniramine, an H1-antagonist, selectively inhibited tracheal contraction to compound 48/80 and histamine. Cimetidine, an H2-antagonist, did not alter the response to intra-arterial histamine. In 11 dogs, the doses of both intra-arterial histamine and acetylcholine required to produce a threshold increase in tracheal tension of 8 g/cm were compared. Threshold doses for acetylcholine varied 10-fold, compared with 100-fold variation for histamine among these dogs. There was a significant correlation between increased tracheal tension produced by compound 48/80 and histamine (r = 0.62). We conclude that compound 48/80 causes a variable increase in tracheal tension in vivo because of marked variability in the H1-receptor response of tracheal smooth muscle to histamine and because of variability in the release of mediator from respiratory mast cells by compound 48/80.

Histamine receptor in bullfrog gastric mucosa

1981 ◽  
Vol 241 (2) ◽  
pp. G93-G97
Author(s):  
S. J. Hersey
Keyword(s):  
Gastric Mucosa ◽  
Histamine Receptor ◽  
Histamine Receptors ◽  
Histamine Antagonists ◽  
Competitive Antagonism ◽  
H2 Antagonist ◽  
H2 Receptors ◽  
High Concentrations ◽  
H1 Antagonist ◽  
Very High

The histamine receptor of isolated bullfrog gastric mucosa was characterized in terms of respiration and acid secretory responses to histamine antagonists and agonists. Cimetidine, a selective H2-antagonist, showed competitive antagonism of histamine responses with a pA2 value of 6.55. In contrast, the H1-antagonist, mepyramine, showed inhibition only at very high concentrations. Based on these results, the histamine receptor would be classified as the H2 type. Measurements of agonist potency sequence revealed a marked difference between the amphibian and mammalian gastric histamine receptors. The selective H1-agonists, 2-pyridylethylamine and 2-aminoethylthiozol, were found to be more efficacious than the selective H2-agonists, dimaprit and impromidine. The lack of efficacy for dimaprit and impromidine does not appear to be due to a lack of binding to the receptor because these agents inhibit responses to histamine. For dimaprit, the inhibition was found to be competitive with an apparent pA2 value of 5.37. These results indicate that there is a molecular difference between H2-receptors in mammals versus amphibians.

Role of arachidonic acid metabolites in ethanol vasoaction in rat gastric submucosa

1988 ◽  
Vol 255 (6) ◽  
pp. G731-G737 ◽  
Author(s):  
Y. Yonei ◽  
H. Wayland ◽  
P. H. Guth
Keyword(s):  
Vessel Diameter ◽  
In Vivo Microscopy ◽  
Lipoxygenase Inhibitor ◽  
Microscopy Technique ◽  
Cyclooxygenase Activity ◽  
Microvascular Response ◽  
Acid Metabolites ◽  
Dose Dependent

By use of an in vivo microscopy technique in the anesthetized rat, the effect of 0.5-8.0% ethanol on gastric submucosal blood vessel diameter was studied. The direct application of ethanol onto the exposed submucosal vasculature caused a dose-dependent dilatation of the arterioles (9 +/- 3% by 2% ethanol) but had no effect on venular diameter. In rats pretreated with 5 mg/kg indomethacin subcutaneously to inhibit cyclooxygenase activity, the submucosal application of ethanol caused dose-dependent constriction of both arterioles and venules (2% ethanol decreasing diameters by 21 +/- 3 and 15 +/- 2%, respectively). This constriction by ethanol in indomethacin-pretreated rats was significantly inhibited by BW755C, a lipoxygenase inhibitor. Under these conditions, 2% ethanol had no significant effect on either arterioles or venules. In conclusion, ethanol appears to cause release of vasodilating prostaglandins and vasoconstricting leukotrienes that may mediate or modulate the microvascular response to ethanol.

Characterization of H1- and H2-receptor function in pulmonary and systemic circulations of sheep

1982 ◽  
Vol 53 (1) ◽  
pp. 175-184 ◽  
Author(s):  
T. Ahmed ◽  
K. B. Mirbahar ◽  
W. Oliver ◽  
P. Eyre ◽  
A. Wanner
Keyword(s):  
Vascular Tone ◽  
Base Line ◽  
H2 Receptor ◽  
Receptor Response ◽  
H2 Antagonist ◽  
H2 Receptors ◽  
H1 Antagonist ◽  
Vasodepressor Response

We investigated the histamine H1- and H2-receptor function in the pulmonary and systemic circulations of sheep by in vivo and in vitro techniques. Combined H1 and H2 stimulation (by intravenous histamine) in vivo increased pulmonary vascular resistance (PVR) to 435% of base line and decreased systemic vascular resistance (SVR) to 49% of base line. Selective H2 stimulation (histamine after chlorpheniramine pretreatment) decreased PVR and SVR to 86 and 82% at base line, respectively, while selective H1 stimulation (histamine after metiamide pretreatment) increased PVR to 424% of base line and decreased SVR to 64% of base line. Combined H1- and H2-antagonist pretreatment completely blocked the effects of histamine on SVR, while PVR still decreased to 85% of base line, suggesting a mild “atypical” H2-receptor response in the pulmonary circulation under conditions of resting vascular tone. With increased pulmonary vascular tone (hypoxia), histamine decreased PVR to 55% (H1-antagonist pretreatment) and to 58% (combined H1- and H2-antagonist pretreatment) of posthypoxia values, respectively, demonstrating a marked atypical H2-receptor response. In vitro, both pulmonary arterial and venous strips showed a contractile dose-response to histamine, which was blocked by the H1-antagonist pyrilamine (mepyramine). In precontracted strips, both histamine and the H2-agonists (dimaprit and impromidine) elicited a relaxant response, which was neither blocked by H1-antagonist alone nor by combined H1- and H2-antagonists. We conclude that in sheep the histamine-induced pulmonary vasoconstrictor response is mediated by H1-receptors, while the pulmonary vasodepressor response is mediated by atypical H2-receptors. The systemic vasodepressor response is mediated by both H1- and typical H2-receptors.

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.

Brain histamine regulates pressor responses to peripheral hyperosmolality

1990 ◽  
Vol 259 (3) ◽  
pp. R507-R513 ◽  
Author(s):  
V. F. Akins ◽  
S. L. Bealer
Keyword(s):  
Pressor Response ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Brain Histamine ◽  
Hypothalamic Region ◽  
Pressor Responses ◽  
H2 Antagonist ◽  
H1 Antagonist ◽  
Dose Dependent

The role of brain histamine (HA) in the pressor response to peripheral hyperosmolality was investigated in the conscious Sprague-Dawley rat. Increased mean arterial pressure was observed during a 30-min intravenous infusion of hypertonic saline (HTS; 10 microliters.100 g body wt-1 x min-1) in vehicle-treated controls (20.1 +/- 3.8 mmHg) and in animals centrally pretreated with the specific H2-antagonist, cimetidine (15.0 +/- 3.7 mmHg). However, this pressor response was abolished in a dose-dependent manner after intracerebroventricular injection of the H1 antagonist promethazine. In other experiments, brain tissue microdissected from the supraoptic nucleus (SON), paraventricular nucleus (PVN), and posterior hypothalamic region showed significantly lower levels of total tissue HA after 60 min of intravenous HTS infusion compared with tissue taken from control animals receiving an isotonic infusion. Microdialysis in the region of the PVN or SON before and during HTS infusion showed increased extracellular concentrations of HA in the SON (24.4 +/- 10.9%) during infusion. No change in extracellular HA concentration was seen in the PVN during HTS infusion. These results support the conclusion that endogenous brain HA is involved in the pressor response to peripheral hyperosmolality.

Biphasic development of pentagastrin sensitivity in rat stomach

1982 ◽  
Vol 242 (2) ◽  
pp. G111-G115
Author(s):  
B. Garzon ◽  
R. Ducroc ◽  
J. P. Onolfo ◽  
J. F. Desjeux ◽  
J. P. Geloso
Keyword(s):  
Acid Output ◽  
Ussing Chamber ◽  
Rat Stomach ◽  
Rat Pups ◽  
Fetal Serum ◽  
Human Gastrin ◽  
Dose Dependent ◽  
Secretion Rates

Rat stomach sensitivity to pentagastrin was examined in fetal (days 19--21) and newborn (5--day-old) preparations in vivo and in vitro. Gastric acidification in vivo was expressed as the gastric content pH and in vitro as the net transepithelial H+ fluxes determined in an Ussing chamber. In both preparations, fetal stomach first responded to pentagastrin on day 20. Dose-dependent H+ secretion was demonstrated in vitro for pentagastrin concentrations of 10(-8) to 10(-6) M, with half-maximal stimulations at 1.9 x 10(-7) and 4 x 10(-7) M on days 20 and 21, respectively. In contrast, isolated fundic mucosa of 5-day-old rat pups exhibited very low H+ secretion rates, and pentagastrin did not significantly stimulate acid output. Fetal serum immunoreactive gastrin was detected as early as day 16 in fairly constant concentrations (about 77.5 pg eq synthetic human gastrin/ml). These results indicate that, although immunoreactive gastrin is present in serum as early as day 165, pentagastrin does nt stimulate acid secretion until day 20 when fetal stomach exhibits active H+ secretion and decreased passive permeability. Pentagastrin sensitivity disappears during the 1st days of extrauterine life. These findings strongly suggest that the development of pentagastrin sensitivity in rat stomach is biphasic.

Involvement of 5-Hydroxytryptamine in Platelet Aggregation In Vivo in Rats and Guinea Pigs

1989 ◽  
Vol 61 (03) ◽  
pp. 463-467 ◽  
Author(s):  
G M Smith
Keyword(s):  
Platelet Count ◽  
Guinea Pigs ◽  
Platelet Adhesion ◽  
Adenosine Diphosphate ◽  
Rate Of Return ◽  
Low Doses ◽  
Dose Dependent ◽  
Higher Doses ◽  
Rat Platelets

SummaryIn this study, 5-hydroxytryptamine (5-HT) caused a dose- dependent fall in the circulating platelet count suggesting that 5-HT receptors are activated in rat platelets to cause platelet adhesion and aggregation. When low doses of adenosine diphosphate (ADP) were simultaneously injected with 5-HT, there was a significant potentiation of the responses to ADR Ketanserin significantly reduced the potentiated responses. When higher doses of ADP were infused with bolus injections of 5-HT there was no potentiation and ketanserin did not reduce these responses. Ketanserin did not inhibit the collagen-induced fall in circulating platelet count, but did significantly increase the rate of return to the basal platelet count compared with control. 5-HT did not cause a fall in platelet count in guinea-pigs

Effects of NO-Donors on Thrombus Formation and Microcirculation in Cerebral Vessels of the Rat

1996 ◽  
Vol 76 (01) ◽  
pp. 111-117 ◽  
Author(s):  
Yasuto Sasaki ◽  
Junji Seki ◽  
John C Giddings ◽  
Junichiro Yamamoto
Keyword(s):  
Blood Flow ◽  
Thrombus Formation ◽  
Dependent Manner ◽  
Red Cell ◽  
Cell Velocity ◽  
Red Cell Velocity ◽  
The Mean ◽  
Wall Shear ◽  
Dose Dependent

SummarySodium nitroprusside (SNP) and 3-morpholinosydnonimine (SIN-1), are known to liberate nitric oxide (NO). In this study the effects of SNP and SIN-1 on thrombus formation in rat cerebral arterioles and venules in vivo were assessed using a helium-neon (He-Ne) laser. SNP infused at doses from 10 Μg/kg/h significantly inhibited thrombus formation in a dose dependent manner. This inhibition of thrombus formation was suppressed by methylene blue. SIN-1 at a dose of 100 Μg/kg/h also demonstrated a significant antithrombotic effect. Moreover, treatment with SNP increased vessel diameter in a dose dependent manner and enhanced the mean red cell velocity measured with a fiber-optic laser-Doppler anemometer microscope (FLDAM). Blood flow, calculated from the mean red cell velocity and vessel diameters was increased significantly during infusion. In contrast, mean wall shear rates in the arterioles and venules were not changed by SNP infusion. The results indicated that SNP and SIN-1 possessed potent antithrombotic activities, whilst SNP increased cerebral blood flow without changing wall shear rate. The findings suggest that the NO released by SNP and SIN-1 may be beneficial for the treatment and protection of cerebral infarction

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