Responses of Human Skin Blood Vessels to Synthetic Histamine Analogues

Robertson, Ivan; Greaves, Malcolm W.

doi:10.1111/j.1365-2125.1978.tb01714.x

Cited by 103 publications

(39 citation statements)

References 5 publications

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“…Human skin blood vessels possess both H, and H; receptors, which are involved in both vasodilation and increased vascular permeability evoked by histamine [16,17]. Treatment with a histamine H, receptor antagonist has been effective in some patients.…”

mentioning

confidence: 99%

Systemic Mastocytosis Treated with Histamine H1 and H2 Receptor Antagonists

Gasior-Chrzan

Folk²

1992

Dermatology

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A case of systemic mastocytosis with skin characteristics of telangiectasia macularis eruptiva perstans is reported. Systemic involvement was confirmed as a combination of highly increased urinary excretion of methyl imidazole acetic acid (Melm AA) and increased amounts of mast cells in skin, liver and colon transversum. Treatment with cimetidine (H₂ receptor antagonist) resulted in diarrhea, however, the addition of cyproheptadine (H₁ receptor antagonist) was beneficial in amelioration of the cutaneous symptoms of mastocytosis. The excretion of Melm AA was unchanged during treatment. After 7 months of continuous cimetidine and cyproheptadine treatment no side effects were observed.

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mentioning

confidence: 99%

Systemic Mastocytosis Treated with Histamine H1 and H2 Receptor Antagonists

Gasior-Chrzan

Folk²

1992

Dermatology

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“…It is possible that the endothelium may inactivate bradykinin (Erdos, 1975). Prolonged treatment with bradykinfi decreased lysosomal fragility, possibily by stimulating endothelial prostaglandin production (Dumonde, Jose, Page & Williams, 1977 Savic & Stoner, 1978;Robertson & Greaves, 1978). Marks & Greaves (1977) have shown that treatment of vascular responses with a combination of HI and H2-antagonists is more effective than with either alone.…”

Section: Introductionmentioning

confidence: 99%

Effects of Inflammatory Agents on Endothelial Lysosomal Fragility and Their Inhibition by Antiinflammatory Drugs

Yoffe

1981

British J Pharmacology

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Endothelial cells from human unbilical veins were maintained in tissue culture. The fragility of lysosomal membranes were studied by microdensitometry. Histamine (50 μm to 10 mm), 4‐methylhistamine (100 nm to 10 mm) and dimaprit (100 nm to 10 mm) increased lysosomal fragility. 2‐Thiazolyethylamine and 2‐pyridylethylamine (100 nm to 10 mm) had no effect. Prostaglandins E1 and E2 (3 nm to 30 μm) and prostaglandin F2α (2 nm to 20 μm) had no direct effect. Low concentrations of prostaglandins E1 and E2 inhibited the fragility induced by histamine 100 μm. Bradykinin (100 nm to 100 μm) decreased fragility. The increase in fragility induced by histamine 100 μm or dimaprit 100 μm was inhibited by cimetidine (100 μm and 1 mm) but not by mepyramine (1 μm to 1 mm). Pretreatment with indomethacin, hydrocortisone, ibuprofen and sodium salicylate caused a dose‐dependent inhibition of histamine‐induced fragility. Threshold concentrations were 1 pm, 100 pm, 10 nm and 10 μm, respectively. Lignocaine (1 μm to 1 mm) had no direct effect and did not decrease histamine‐induced fragility.

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“…These mast cell mediators increase vascular permeability, and promote leakage of intra vascular proteins into the submucosa and nasal secre tions [6][7][8]. In addition, selective mediators released during the early phase are chemotactic for inflamma tory cells.…”

Section: Introductionmentioning

confidence: 99%

Nasal Inflammatory Mediator Release in Ragweed Allergic Rhinitis: Correlation with Cellular Influx into Nasal Secretions

Georgitis

Stone²,

Gottschlich³

1991

Int Arch Allergy Immunol

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Lipid-derived mediators are found in nasal secretions during the early and late phase of allergic responses. To explore this early response further, concentrations of inflammatory mediators were measured along with characterization of specific cell influx during dose-dependent ragweed challenges. Ten allergic rhinitis subjects underwent two unilateral nasal lavages using 3-fold concentrations of short ragweed antigen. Low doses of ragweed (0.016–0.114 units Amb a I) did not provoke cell influx (1 of 18 challenges), whereas moderate doses (0.432–1.3 units Amb a I) induced cell influxes in 7 of 18 and at high doses in 8 of 17 challenges (3.39–11.7 units Amb a I). The differential of the cellular influx was > 50% neutrophils in 7 challenges; > 50% eosinophils in 3, and a mixed pattern in 6. There was a significant association between the dose of antigen and the level of prostaglandin D₂ (PGD₂), leukotrienes (LTs) C₄, D₄ and E₄. Challenges with an eosinophilic influx tended to be associated with higher concentrations of mediators than neutrophilic influxes. Similar to the immediate skin response, the early allergic response in the nose demonstrated a cell influx with release of PGD₂, LTsC₄, D₄ and E₄. Nasal cellular inflammation therefore can occur within minutes of allergen exposure.

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Responses of Human Skin Blood Vessels to Synthetic Histamine Analogues

Cited by 103 publications

References 5 publications

Systemic Mastocytosis Treated with Histamine H<sub>1</sub> and H<sub>2</sub> Receptor Antagonists

Systemic Mastocytosis Treated with Histamine H<sub>1</sub> and H<sub>2</sub> Receptor Antagonists

Effects of Inflammatory Agents on Endothelial Lysosomal Fragility and Their Inhibition by Antiinflammatory Drugs

Nasal Inflammatory Mediator Release in Ragweed Allergic Rhinitis: Correlation with Cellular Influx into Nasal Secretions

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