STUDIES ON THE MECHANISM OF NIDATION: X.

1964 ◽  
Vol 47 (2) ◽  
pp. 255-264 ◽  
Author(s):  
G. J. Marcus ◽  
M. C. Shelesnyak ◽  
P. F. Kraicer
Keyword(s):  
Histamine Release ◽  
Significant Degree ◽  
Histamine Level ◽  
Histamine Content ◽  
Rat Uterus ◽  
Sequence Of Events ◽  
No Release ◽  
Significant Release ◽  
In Pregnancy

ABSTRACT Accumulated evidence suggested the occurrence of the following sequence of events in nidation in the rat: An oestrogen-surge, occurring on day L3 of pregnancy, releases histamine in the uterus; the liberated histamine stimulates the progestational endometrium, inducing decidualization. Since an oestrogen-surge occurs also during pseudopregnancy, the same sequelae, culminating in decidualization, are to be invariably expected. The present study was undertaken to determine the basis for the rarity of spontaneous decidualization in the pseudopregnant rat. Measurement of day to day changes in the histamine content of the rat uterus confirmed the occurrence of histamine-release following the oestrogen-surge of pregnancy. During pseudopregnancy, however, following the histamine decline after oestrus, a high histamine level is not re-established as in pregnancy but the histamine content remains low and no release is observed after the oestrogen-surge of pseudopregnancy. Supplementing the surge oestrogen with exogenous oestradiol or oestriol in doses as great as 40 μg failed to induce a significant degree of decidualization in the pseudopregnant rat, indicating that no significant release of histamine was induced. The rarity of spontaneous decidualization in the pseudopregnant rat therefore is due to the absence of a pool of histamine amenable to release by oestrogen. It is, therefore, apparent that hormonal influences on the uterus are not identical in pseudopregnancy and in pregnancy.

Effect of hypothermia on histamine release induced by epinephrine infusion

1960 ◽  
Vol 199 (2) ◽  
pp. 272-274 ◽  
Author(s):  
T. Szilagyi ◽  
A. Kover ◽  
B. Csaba
Keyword(s):  
Histamine Release ◽  
Femoral Artery ◽  
Saphenous Vein ◽  
Histamine Level ◽  
Histamine Content ◽  
Epinephrine Infusion

Experiments were performed on dogs anesthetized with chloralose. Epinephrine was infused (20 µg/kg/min.) into the saphenous vein and blood was taken from the femoral artery. Diffusible histamine contents of the plasma were estimated with the superfusion method. It was found that in normothermia epinephrine infusion results in a considerable rise of histamine level. After the cooling of the animals (21.5°–23°C) histamine release does not take place at all during and after the epinephrine infusion, and the histamine content of the blood does not change.

scholarly journals Glucagon Effects on3H-Histamine Uptake by the Isolated Guinea-Pig Heart during Anaphylaxis

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Mirko Rosic ◽  
Oberdan Parodi ◽  
Vladimir Jakovljevic ◽  
Maja Colic ◽  
Vladimir Zivkovic ◽  
...  
Keyword(s):  
Free Radicals ◽  
Guinea Pig ◽  
Histamine Release ◽  
Coronary Circulation ◽  
Histamine Level ◽  
Guinea Pig Heart ◽  
Cardiac Anaphylaxis ◽  
Endogenous Histamine ◽  
No Release ◽  
Histamine Uptake

We estimated the influence of acute glucagon applications on3H-histamine uptake by the isolated guinea-pig heart, during a single3H-histamine passage through the coronary circulation, before and during anaphylaxis, and the influence of glucagon on level of histamine, NO,O2-, and H2O2in the venous effluent during anaphylaxis. Before anaphylaxis, glucagon pretreatment does not change3H-histamine Umax and the level of endogenous histamine. At the same time, in the presence of glucagon,3H-histamine Unet is increased and backflux is decreased when compared to the corresponding values in the absence of glucagon. During anaphylaxis, in the presence of glucagon, the values of3H-histamine Umax and Unet are significantly higher and backflux is significantly lower in the presence of glucagon when compared to the corresponding values in the absence of glucagon. The level of endogenous histamine during anaphylaxis in the presence of glucagon (6.9–7.38 × 10−8 μM) is significantly lower than the histamine level in the absence of glucagon (10.35–10.45 × 10−8 μM). Glucagon pretreatment leads to a significant increase in NO release (5.69 nmol/mL) in comparison with the period before glucagon administration (2.49 nmol/mL). Then, in the presence of glucagon,O2-level fails to increase during anaphylaxis. Also, our results show no significant differences in H2O2levels before, during, and after anaphylaxis in the presence of glucagon, but these values are significantly lower than the corresponding values in the absence of glucagon. In conclusion, our results show that glucagon increases NO release and prevents the increased release of free radicals during anaphylaxis, and decreases histamine level in the venous effluent during cardiac anaphylaxis, which may be a consequence of decreased histamine release and/or intensified histamine capturing by the heart during anaphylaxis.

STUDIES ON THE MECHANISM OF NIDATION. XXXIII.

1968 ◽  
Vol 57 (1) ◽  
pp. 136-141 ◽  
Author(s):  
G. J. Marcus ◽  
M. C. Shelesnyak
Keyword(s):  
Histamine Release ◽  
Seminal Plasma ◽  
Histamine Content ◽  
Rat Uterus ◽  
Pregnant Rat ◽  
Low Level ◽  
Level Characteristic ◽  
Electrical Induction

ABSTRACT In an extension of previous studies which had shown that decidual induction in the rat depends on the availability of histamine, the possibility that exposure of the rat uterus to semen influences the availability of histamine in the uterus was investigated. The histamine content of the rat uterus was measured following normal mating (uterus exposed to seminal plasma plus sperm), following mating with vasectomized males (uterus exposed to seminal plasma only) and following electrical induction of pseudopregnancy. Mating with vasectomized males resulted in an elevation of the histamine content of the uterus from the low level characteristic of electrically induced pseudopregnancy to approximately the level characteristic of pregnancy in the preimplantation period. Histamine-release, which occurs at the time of decidual induction in the pregnant rat, did not occur in the uterus of the rats mated with vasectomized males. The elevation in histamine following mating was attributed to importation by cells infiltrating the uterus in response to the stimulus of mating. The non-release of histamine was attributed to the lack of stimulation in the absence of the blastocyst.

Antagonists of LHRH with Histidine in the Priority Position 8

1993 ◽  
Vol 48 (6) ◽  
pp. 812-816 ◽  
Author(s):  
Anna Janecka ◽  
Si-Mei Shan ◽  
Cyril Bowers ◽  
Karl Folkers
Keyword(s):  
Luteinizing Hormone ◽  
Histamine Release ◽  
Side Effect ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Significant Release ◽  
Potent Antagonist ◽  
Antiovulatory Activity

Sixteen new designs of antagonists of the luteinizing hormone releasing hormone (LHRH) with histidine in position 8 were synthesized, because this position is critical both for antiovulatory activity and the side effect of histamine release. The most potent antagonist was NAcDQal-DpClPhe–D 3 Pal– Ser–cPzACAla–DPicLys– Leu– His – Pro –DAlaNH2, which showed 33% AOA at 0.25 μg. The histamine release was remarkably negligible by an ED50 of 308 μg/ml which is superior to 186 μg/ml for LHRH and comparable to 300 for Antide.The relative basicities of His, Arg, and ILys in position 8 of antagonists appear to influence both the level of potency of AOA and a negligible to a significant release of histamine. The least basic His8-analogs can have the lowest AOA and the highest ED50. The very basic Arg8-analogs can have the highest AOA and the lowest ED50. The moderately basic ILys8-analogs can be a compromise for acceptable levels of potency and safety.

Platelet Proteins Cause Allergic Transfusion Reactions through an Immunoglobulin-Dependent Mechanism

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 91-91
Author(s):  
Dong-Young Donna Lee ◽  
Igla Muskaj ◽  
William Savage
Keyword(s):  
Cell Surface ◽  
Histamine Release ◽  
Small Molecules ◽  
Platelet Lysate ◽  
Histamine Content ◽  
Heat Denaturation ◽  
Mild Heat ◽  
Healthy Donors ◽  
Dnase Treatment ◽  
Basophil Cell

Abstract Background: A general understanding of allergic transfusion reaction (ATR) mechanisms remains elusive. Various hypotheses invoke proteins, small molecules, mitochondria, or microparticles that may be plasma or platelet derived and suggest antibody dependent or independent mechanisms. There has been no systematic comparison of these proposed mechanisms. The aim of this study is to characterize the mechanistic determinants of ATRs. Methods: Basophil enriched cell suspensions were collected from healthy donors (n=8). Basophil histamine release was measured in response to platelet-derived components: platelet component supernatant (plasma), platelet lysate, and manipulated platelet lysates were examined to characterize the unknown allergic stimuli. Lysate manipulations were: 1) dialysis against a 3,500 molecular weight cutoff membrane, 2) butanol/DIPE delipidation, 3) trypsinization with immobilized trypsin beads, 4) mild heat denaturation at 47˚C for 20 minutes, and 5) ultracentrifugation at 200,000 gfor 1hr. Immunoglobulin-dependent mechanisms were investigated through lactic acid immunoglobulin depletion from the basophil cell surface and signaling inhibition with ibrutinib. Histamine release from magnetic bead isolated platelet mitochondria was compared to platelet lysate with or without DNase treatment. Platelet lysate histamine content represented an average of <4% of total basophil histamine content. The residual histamine originating from platelet lysate was subtracted from post-reaction histamine concentrations. Atopic histories and grass, tree, and weed-specific IgE were measured in basophil donors. Results: Robust, dose-responsive histamine release to platelet lysate was observed in two of eight healthy donors. No histamine release was observed with plasma. Reactivity did not correlate with the clinical allergic phenotype, and reactive donors were nulliparous and had no prior transfusion. Trypsin treatment of platelet lysate reduced histamine release by 39% (p=0.008). Delipidation of platelet lysate decreased histamine release by 20% (p=0.051). Dialysis, ultracentrifugation, and mild heat denaturation of platelet lysate did not significantly affect histamine release, compared to unmanipulated platelet lysate. To investigate the immunoglobulin dependence of basophil activation, in separate experiments we 1) depleted immunoglobulins, including IgE, from the basophil cell surface, and 2) inhibited immunoglobulin-mediated intracellular signaling with ibrutinib. Histamine release in response to platelet lysate significantly decreased in both cases. Finally, isolated platelet mitochondria induced minimal basophil histamine release, and DNase treatment did not inhibit activation of basophils by platelet lysate. Conclusion: Type I immediate hypersensitivity to platelet, not plasma, proteins is a primary mechanism for ATRs. Small molecules, microparticles, and mitochondria are not significant contributors to ATRs in this human basophil model. Prior sensitization to human proteins is not required for basophil responses to platelet proteins. Donor variability and storage conditions that promote accumulation of soluble platelet-derived proteins may contribute to ATRs. Disclosures No relevant conflicts of interest to declare.

scholarly journals LEUKOCYTE-DEPENDENT HISTAMINE RELEASE FROM RABBIT PLATELETS

1972 ◽  
Vol 136 (6) ◽  
pp. 1356-1377 ◽  
Author(s):  
Jacques Benveniste ◽  
Peter M. Henson ◽  
Charles G. Cochrane
Keyword(s):  
Histamine Release ◽  
Platelet Activating Factor ◽  
Histamine Content ◽  
Immediate Hypersensitivity ◽  
Rabbit Platelets ◽  
Independent Mechanism ◽  
Immunologic Disease ◽  
Structural Injury ◽  
Aggregation Of Platelets ◽  
Dependent Mechanism

We have studied the leukocyte-dependent mechanism of histamine release (LDHR) from rabbit platelets, a complement-independent mechanism which has been implicated in the deposition of immune complexes in acute serum sickness of rabbits. It was found by chromatography and passive transfer of serum from immunized rabbits that the antibody responsible for the LDHR was of IgE type. By electron microscope study of the reaction, the leukocyte involved in agglutination of platelets and release of their histamine content was identified as the basophil. Upon addition of antigen, basophils sensitized with IgE degranulated, released their histamine content and a platelet-activating factor (PAF) that caused aggregation of platelets and release of their histamine. Conditions of preparing and preserving PAF activity and some properties of this factor have been elucidated. LDHR must, therefore, be considered as an immediate hypersensitivity-type mechanism which may link allergic reactions with immunologic disease associated with severe structural injury.

scholarly journals The antineoplastic bryostatins affect human basophils and mast cells differently

Blood ◽  
1995 ◽  
Vol 85 (5) ◽  
pp. 1272-1281 ◽  
Author(s):  
V Patella ◽  
V Casolaro ◽  
A Ciccarelli ◽  
GR Pettit ◽  
M Columbo ◽  
...  
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Bryostatin 1 ◽  
Histamine Secretion ◽  
Gm Csf ◽  
Protein Kinase C Inhibitors ◽  
Therapeutic Trials ◽  
Heterogeneous Effects ◽  
No Release ◽  
Human Basophils

Bryostatins, macrocyclic lactones from the marine bryozoan Bugula neritina, are potent antineoplastic agents and multi-potential stimulators of immune cells. We have examined the effects of bryostatins on mediator release from human basophilic leukocytes and human tissue mast cells. Bryostatins 1, 2, and 5 (10 to 3,000 nmol/L) induced histamine secretion from purified and unpurified peripheral blood basophils, whereas they caused no release of peptide-leukotriene C4 from these cells. The rate of histamine release caused by bryostatin 1 was slower than that caused by anti-IgE (t1/2 +/- SEM = 38.2 +/- 4.7 minutes v 8.9 +/- 0.2 minutes; P < .01), whereas the temperature dependence was similar (optimum release at 37 degrees C, approximately 30% less at 30 degrees C, and no release at 22 degrees C or 4 degrees C). The addition of increasing concentrations of extracellular Ca2+ to the medium caused histamine release in the presence of bryostatins. Subeffective concentrations of bryostatins and anti-IgE produced a synergistic effect on histamine release from basophils. Staurosporine, chelerythrine, and calphostin C (0.1 to 10 nmol/L), which are protein kinase C inhibitors, inhibited the histamine secretion activated by bryostatin 1 and tetradecanoylphorbol-acetate (TPA). Preincubation with granulocyte-monocyte colony-stimulating factor (GM-CSF; 1 and 5 nmol/L) and interleukin-3 (IL-3; 10 ng/mL) potentiated the activation of human basophils induced by bryostatin 1. Neither bryostatin 1 nor bryostatin 2 induced the release of histamine from mast cells isolated from human lung or skin tissues. However, brief (10 minutes) preincubation with bryostatin 1 (3 to 300 nmol/L) potently inhibited the histamine secretion induced by anti-IgE from skin or lung mast cells. Bryostatin 1 was a more potent (by approximately 30 times) inhibitor of IgE- mediated histamine release than was TPA. The heterogeneous effects exerted by bryostatins on human basophils and mast cells can be of interest for those designing therapeutic trials using these agents.

Sign in / Sign up

Export Citation Format

Share Document