Effect of H1-antagonist Dithiaden® on human PMN-leukocyte aggregation and chemiluminescence is stimulus-dependent

2002 ◽  
Vol 51 (11) ◽  
pp. 557-562 ◽  
Author(s):  
R. Nosál ◽  
K. Drábiková ◽  
M. Čiž ◽  
A. Lojek ◽  
E. Danihelová
Keyword(s):  
Leukocyte Aggregation ◽  
Pmn Leukocyte ◽  
H1 Antagonist

Membrane Changes in Polymorphonuclear Leukocytes During Ionophore (A23187) - Induced Lysosomal Release

1977 ◽  
Vol 35 ◽  
pp. 482-483
Author(s):  
P.L. Moore ◽  
P.L. Sannes ◽  
H.L. Bank ◽  
S.S. Spicer
Keyword(s):  
Structural Changes ◽  
Calcium Release ◽  
Clear Understanding ◽  
Ionophore A23187 ◽  
Enzyme Release ◽  
Extracellular Medium ◽  
Pmn Leukocytes ◽  
Intracellular Ion Concentrations ◽  
Membrane Changes ◽  
Pmn Leukocyte

It is thought that calcium and/or magnesium may play important roles in polymorphonuclear (PMN) leukocyte functions such as chemotaxis, adhesion and phagocytosis. Yet, a clear understanding of the biological roles of these ions has awaited the development of techniques which permit a selective alteration of intracellular ion concentrations. Recently, treatment of cells with the ionophore A23187 has been used to alter intracellular divalent cation concentrations. This ionophore is a lipid soluble antibiotic produced by Streptomyces chartreusensis that complexes with both calcium and magnesium (3) and is believed to carry these ions across biological membranes (4). Biochemical investigations of human PMN leukocytes demonstrate that cells treated with A23187 and extracellular calcium release their lysosomal enzymes into the extracellular medium without rupturing and releasing their soluble cytoplasmic enzymes (5,6). The aim of the present study and and a companion report (7) was to investigate the structural changes that occur in leukocytes during ionophore-induced lysosomal enzyme release.

The histamine H1-antagonist chlorpheniramine facilitates learning in aged rats

1997 ◽  
Vol 229 (2) ◽  
pp. 89-92 ◽  
Author(s):  
Christian Frisch ◽  
Rüdiger U. Hasenöhrl ◽  
Joseph P. Huston
Keyword(s):  
Aged Rats ◽  
H1 Antagonist

The effects of hydrogen sulfide on platelet–leukocyte aggregation and microvascular thrombolysis

Platelets ◽  
2016 ◽  
Vol 28 (5) ◽  
pp. 509-517 ◽  
Author(s):  
Eberhard Grambow ◽  
Christian Leppin ◽  
Katja Leppin ◽  
Günther Kundt ◽  
Ernst Klar ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Leukocyte Aggregation

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.

Potent vasoactive properties of endothelin 1 in human skin

1991 ◽  
Vol 70 (1) ◽  
pp. 260-266 ◽  
Author(s):  
D. C. Crossman ◽  
S. D. Brain ◽  
R. W. Fuller
Keyword(s):  
Blood Flow ◽  
Endothelial Cell ◽  
Human Skin ◽  
Intradermal Injection ◽  
Local Response ◽  
Axon Reflex ◽  
Endothelin 1 ◽  
Calcitonin Gene ◽  
H1 Antagonist ◽  
Dose Dependent

The effect of the endothelial cell-derived peptide endothelin 1 was investigated in human skin. Intradermal injection of endothelin 1 (1–100 pmol) caused a dose-dependent area of pallor that was associated with a significant reduction in basal skin blood flow, measured by laser-Doppler blood flowmeter (with 1 pmol endothelin, P = 0.012, analysis of variance). The coadministration of endothelin 1 (1–100 pmol) with the neuropeptide vasodilator calcitonin gene-related peptide (CGRP) inhibited the vasodilator response to CGRP (10 pmol) by up to 82.7 +/- 9.2% (with 100 pmol endothelin, P less than 0.001). The response of the prostanoid vasodilator prostaglandin E2 (10 pmol) was inhibited by endothelin in a similar manner. In addition to the vasoconstrictor effects, endothelin 1 produced a dose-dependent flare that surrounded the area of pallor, and this was associated with a significant increase in blood flow (P less than 0.05) within the flare area. The H1 antagonist terfenadine (120 mg po) significantly reduced the flare area associated with endothelin 1: flare 5 min after intradermal endothelin (10 pmol, placebo treated), 668 +/- 405 mm2; terfenadine treated, 201 +/- 257 mm2 (P less than 0.05). The flare was also significantly attenuated when endothelin (10 pmol) was injected into local anesthetic-treated skin. Thus intradermal injection of endothelin in humans causes long-lasting vasoconstriction at the site of injection and a surrounding flare. Results suggest that the flare component is partially histamine dependent and the result of an axon reflex. This study demonstrates the potent activity of endothelin in human skin. It is possible that endothelin could be relevant to the local response of skin to injury.

P-Selectin-β2-Integrin Cross-Talk: A Molecular Mechanism For Polymorphonuclear Leukocyte Recruitment At The Site Of Vascular Damage

1999 ◽  
Vol 82 (08) ◽  
pp. 787-793 ◽  
Author(s):  
Virgilio Evangelista ◽  
Giovanni de Gaetano ◽  
Chiara Cerletti
Keyword(s):  
Cross Talk ◽  
Molecular Mechanisms ◽  
Vascular Damage ◽  
Tissue Integrity ◽  
Β2 Integrin ◽  
Leukocyte Accumulation ◽  
Platelet Thrombus ◽  
And Migration ◽  
The One ◽  
Pmn Leukocyte

IntroductionPlatelets activated at the site of vascular damage play a pivotal role in polymorphonuclear (PMN) leukocyte accumulation in a growing thrombus2,3 and may substitute endothelial cells in the recruitment and migration of leukocytes through damaged vessel wall.4 Leukocytes, accumulated in a platelet thrombus, can contribute to further platelet activation5 and to increased fibrin deposition.6 These events, on the one hand, may contribute to the maintenance of vascular and tissue integrity. They may, however, play a pathogenic role in inflammatory and thrombotic disease, providing some biological plausibility to the epidemiological evidence of significant association between leukocyte count and the incidence of coronary heart disease.7,8 We shall focus our attention on the molecular mechanisms involved in the recruitment of PMN leukocytes on activated platelets as it occurs at the site of vascular damage, with particular attention to P-selectin- β2-integrin cross-talk.

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