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Biomedical subjects

M W Greaves

Publications and source records attributed to M W Greaves.

At least 217 records · Page 12Linked to original sources
PubMed1983

Increased concentrations of arachidonic acid, prostaglandins E2, D2, and 6-oxo-F1 alpha, and histamine in human skin following UVA irradiation.

The buttock skin of clinically normal human subjects was subjected to approximately 2.5 minimal erythema doses of ultraviolet A irradiation. Deep red erythema developed during irradiation, faded slightly within the next few hours, increased to maximum intensity between 9-15 h, and decreased gradually thereafter although still persisting strongly at 48 h. Suction blister exudates were obtained at 0, 5, 9, 15, 24, and 48 h after irradiation as well as suction blister exudates from a contralateral control site and assayed for arachidonic acid, prostaglandins D2 and E2, and the prostacyclin breakdown product 6-oxo-prostaglandin F1 alpha by gas chromatography-mass spectrometry, and for histamine by radioenzyme assay. Increased concentrations of arachidonic acid and prostaglandins D2, E2, and 6-oxo-prostaglandin F1 alpha were found maximally between 5-9 h after irradiation, preceding the phase of maximal erythema. Elevations of histamine concentration occurred 9-15 h after irradiation, preceding and coinciding with the phase of maximal erythema. At 24 h, still at the height of the erythemal response, all values had returned to near control levels. Hence increased concentrations of arachidonic acid and its products from the cyclooxygenase pathway, and of histamine, accompany the early stages up to 24 h. A causal role in production of the erythema seems likely for these substances although other mediators are almost certainly involved.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Arachidonic acid and prostaglandin levels in dithranol erythema: time course study.

Arachidonic acid and prostaglandins were measured in uninvolved psoriatic skin before and after treatment for up to 24 h with dithranol. Prior to treatment, skin exudate contained 2744 ng ml-1 arachidonic acid and 26.4 ng ml-1 PGE2. After treatment with dithranol, the arachidonic acid concentration increased to a maximum of 5556 ng ml-1 at 48 h whilst PGE2 increased to 93.4 ng ml-1 at 12 h and then declined. The erythemal response was apparent at 6-12 h and maximal at 72 h. These results suggest that PGE2 mediates the early development of dithranol erythema.

Adult↗
PubMed1983

Relationship between skin type and erythemal response to anthralin.

Anthralin erythema dose-response curves were drawn for thirty adult patients of various skin types who had chronic plaque psoriasis. A small statistically significant difference was observed between the curves for skin types I and IV but this was not thought to be sufficient to account for the clinical impression of increased anthralin irritancy in fair-skinned subjects.

Adult↗
PubMed1983

Persisting cholinergic erythema: a variant of cholinergic urticaria.

A new variant of cholinergic urticaria is described. Four patients each had a similar persistent macular skin rash distributed maximally over the upper limbs and upper trunk. Though the rash was persistent, individual macules were of short duration but new macules continually appeared at adjacent sites. Exercise and hot baths exacerbated pruritus and provoked lesions in previously unaffected areas. Topically applied benzoyl scopolamine blocked the appearance of the lesions after challenge. Tests of cholinergic function were normal, apart from an exaggerated pupillary response to arecoline in one patient.

Acetylcholine↗
PubMed1983

Responses of human skin to intradermal injection of leukotrienes C4, D4 and B4.

The ability of intradermally injected leukotrienes C4 (LTC4), LTD4 and LTB4 to produce inflammatory changes in human skin alone and in combination with prostaglandin E2 (PGE2) has been investigated. LTC4 and D4 (0.012-0.38 nmol) caused dose-related erythema and wealing. No evidence of synergism between PGE2 and LTC4 or LTD4 was detected, although only single dose combinations were studied. LTB4 (0.15-1.5 nmol) caused areas of induration which persisted for more than 4 h and which showed perivascular neutrophil infiltrates on histological examination. Only slight synergism between PGE2 and LTB4 was found. It was concluded that these pro-inflammatory properties of LTC4, LTD4 and LTB4 are consistent with their proposed roles as mediators of inflammation in the skin and other tissues.

Adult↗
PubMed1983

Histamine and the skin.

The role of histamine in urticaria is reviewed with particular reference to experiments on cold contact urticaria. In this model, histamine release clearly has a central role, but the failure of drugs which suppress histamine release to alleviate symptoms, other than itching, suggests that other pharmacological agents must be involved. Evidence is presented that prostaglandin E may play a role in some of these patients. The discovery that human blood vessels possess H2 receptors as well as H1 receptors is discussed with particular reference to the role of combined H1 and H2 pharmacological blockade.

Albuterol↗
PubMed1983

Arachidonic acid metabolites and the skin.

The relevance of arachidonic acid metabolites in inflammatory skin diseases has been expanded by recent developments in analytical chemistry. The metabolites include prostaglandins, leukotrienes and monohydroxy fatty acids. In ultraviolet light-induced inflammation the concentrations of arachidonic acid, prostaglandin E2, prostaglandin F2 alpha and 6-oxo-prostaglandin F1 alpha are elevated. Indomethacin totally suppresses the evoked prostaglandin increase, but erythema is only partially suppressed. This indicates that prostaglandins are partially involved in erythema production. In psoriasis the first histological change is an infiltration into the epidermis by neutrophilic leucocytes. It has been suggested that chemotactic factors, such as complement derived factors or leukotriene B4 play a role in the pathogenesis of psoriasis.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1982

Levels of prostaglandins and arachidonic acid in UV-B irradiated human skin before and after topical application of benzyl-2,5-diacetoxybenzoate, a salicylic acid derivative.

Benzyl-2,5-diacetoxybenzoate (BDAB) was tested for anti-inflammatory activity on experimentally inflamed skin. Human abdominal skin was irradiated with three minimal erythema doses of UV-B (290-320nm) radiation to give a maximum erythema at 24 hours with an associated rise in PGE2 and PGF2 alpha levels measured by gas chromatography-mass spectrometry. Topical application of a 1% w/w preparation of BDAB neither decreased the evoked erythema nor diminished the rise in PGE2 and PGF2 alpha concentrations. BDAB, applied topically, was judged to be ineffectual as an anti-inflammatory agent in UV-B erythema.

Aged↗
PubMed1982

Increased levels of 6-oxo-PGF1 alpha in human skin following ultraviolet B irradiation.

1 Clinically normal human abdominal skin in 11 subjects, was irradiated with three times the minimal-erythema dose of ultraviolet B (u.v. B) irradiation. 2 Erythema was assessed visually, and exudate was recovered by a suction bulla technique from normal skin, and from skin at 6, 24 and 48 h after irradiation. 3 Erythema was moderate at 6 h, but increased to a maximum at 24 h, which was maintained at 48 h. 4 6-oxo-PGF1 alpha was markedly raised at 6 h, moderately raised at 24 h, but had returned to control levels at 48 h, when the erythema was still maximal. 5 Prostaglandin I2, the precursor of 6-oxo-PGF1 alpha and 6-oxo-PGF1 alpha may, therefore, play a part in the early inflammatory process after u.v. B irradiation, but is unlikely to be responsible for the erythema still present at 48 h.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

The effect of systemic prednisolone on arachidonic acid, and prostaglandin E2 and F2 alpha levels in human cutaneous inflammation.

1 In order to test the proposal that the anti-inflammatory effect of corticosteroids is attributable to inhibition of release of the prostaglandin precursor, arachidonic acid, the effect of systemic prednisolone on arachidonic acid and prostaglandin levels in abdominal skin of six patients receiving this treatment for alopecia totalis, was studied. 2 Inflammation was produced in an area of abdominal skin by topical application of 5% w/w tetrahydrofurfuryl nicotinate (THFN) cream. 3 The erythema produced was assessed visually, and exudate recovered from normal and inflamed skin, by a suction bulla technique. 4 Arachidonic acid and PGE2 and PGF2 alpha levels, as measured by gas chromatograph-mass spectrometry (GC-MS) were significantly elevated in the reddened (THFN) treated skin, compared with control areas. 5 After prednisolone treatment both arachidonic acid and prostaglandin levels in THFN-treated areas were suppressed near to values obtained from untreated skin, before prednisolone therapy. There was partial reduction of THFN induced erythema in three out of six subjects. Levels of arachidonic acid on control skin were not affected by the steroid. 6 These results provide direct evidence that steroids inhibit prostaglandin formation by blocking evoked rise in the concentration of free arachidonic acid. The relationship of this effect, in human skin, to the anti-inflammatory action of systemic steroids is uncertain.

Adolescent↗
PubMed1982

Histamine receptors in human skin: indirect evidence.

Use of differential effects of agonists and antagonists has provided an experimental basis for subdivision of histamine receptors into H1 and H2. This has enabled classification of the responses to histamine in a wide range of organs and tissues. In human skin the vascular and sensory effects of histamine have been studied, and the influence of histamine on epidermal cell growth has been evaluated in vitro. The direct vasodilator and vascular permeability actions of histamine appear to involve both H1 and H2 receptors. However, the axon reflex flare due to histamine appears to be predominantly an H1 effect. Histamine itch involves H1 receptors. These findings have prompted clinical evaluation of combined therapy with H1 and H2 antagonists in patients with urticaria. Initial results have been encouraging in patients with factitious urticaria. Histamine exerts an inhibitory action on epidermopoiesis in vitro in a number of mammalian epidermal cell outgrowth systems including human explants. The pathophysiological relevance of this effect, which involves epidermal H2 receptors and which may be cyclic AMP dependent, is unknown.

Capillary Permeability↗