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Biomedical subjects

G B West

Publications and source records attributed to G B West.

At least 37 records · Page 2Linked to original sources
PubMed1983

Histamine release by phosphatidic acid from isolated mast cells of two types of genetically different rats.

Phosphatidic acid produced a similar dose-dependent release of histamine from isolated peritoneal mast cells of two types of rat, one of which did not release histamine when dextran was present in the incubation mixture. This release induced by phosphatidic acid resembled that evoked by a basic secretagogue like compound 48/80, being independent of exogenous calcium and unaffected by either phosphatidyl serine or its lyso derivative. The non-cytotoxic release of histamine induced by phosphatidic acid is therefore distinct from that by dextran and does not involve dextran receptors residing on the plasma membrane of mast cells of rats which show the dextran anaphylactoid reaction.

Animals↗
PubMed1983

Proteins in the plasma membranes of rat peritoneal mast cells.

Plasma membranes of peritoneal mast cells from rats specifically bred for resistance to the dextran anaphylactoid reaction contain a polypeptide of molecular weight about 74,000 daltons which is deficient in those from rats which react to dextran. This polypeptide may modify the dextran receptor on the mast cell membranes of resistant rats so that histamine release does not take place when these cells are challenged with clinical dextran.

Animals↗
PubMed1983

Heparin and the dextran anaphylactoid reaction in rats.

Injections of heparin had no effect on the dextran anaphylactoid reaction in rats but neutralised the inhibitory action both of protamine and of borate. Heparin, protamine, and borate did not modify the histamine or 5-hydroxytryptamine responses in rat paws and so their effects on dextran may be due to modification of the release mechanisms of these two amines from tissue mast cells.

Anaphylaxis↗
PubMed1983

Enhancement of the anaphylactoid reaction in rats by phenylalanine enamine.

Low doses of phenylalanine enamine, administered at the same time as dextran, significantly enhanced the onset, height and duration of the anaphylactoid reaction in rats. The enhancement occurred after intraperitoneal or local administration. The enamine did not modify the histamine or 5-hydroxytryptamine responses in rat paws, so its effect on dextran may be due to modification of the release mechanism of the two amines from tissue mast cells.

Adjuvants, Immunologic↗
PubMed1983

Histamine releasers and rat mast cells.

The release of histamine from rat tissues rich in mast cells, induced by antigen, concanavalin A, dextran, compound 48/80, A 23187, phosphatidic acid and chlortetracycline, has been compared with that from isolated peritoneal mast cells of rats. Whereas most of the agents were more active than dextran in in vitro experiments, the reverse was found when they were injected intradermally into the skin, or subcutaneously into the paws. In fact, A 23187 and chlortetracycline (both calcium ionophores), as well as phosphatidic acid (another non-cytotoxic releaser), failed to release significant amounts of histamine when injected into the animal. Thus, the experimental conditions in which comparisons of the activities of histamine releasers are made should always be stated.

Animals↗
PubMed1982

Histamine release from isolated and intact mast cells of two types of genetically different rat.

A comparison has been made of the release of histamine from tissues of conventional rats, induced by injections of antigen, concanavalin A and clinical dextran, with that from rat isolated peritoneal mast cells. Concanavalin A was less active than dextran when injected into the skin or paws, but the reverse was found when the substances were tested on isolated cells. Similar results were obtained when a pure line of rats relatively resistant to dextran was used, concanavalin A being much more active on isolated cells than on intact mast cells. Antigen was equally active in the two types of rat. It is important, therefore, to state the experimental conditions when comparisons of the activities of histamine releasers are being made.

Animals↗
PubMed1982

Testing for drugs inhibiting the formation of gastric ulcers.

Copper salicylate has been shown to be an inhibitor of gastric lesions in rats induced by aspirin, indomethacin and cold stress whereas cimetidine was only effective against those produced by cold stress. The results are in line with those reported earlier for the anti-ulcer activity of sodium salicylate and metiamide respectively. On this basis, it appears that the animal model of stress-induced gastric lesions in the rat is the most suitable for testing the activity of new-antiulcer drugs.

Animals↗
PubMed1982

Effects of levamisole and D-penicillamine on contact sensitivity to oxazolone in rats.

Levamisole, but not D-penicillamine, inhibited the oxazolone delayed hypersensitivity in rats. It was more effective when given locally to the ear (the tissue being challenged with oxazolone) or when injected intraperitoneally 24 h previously. Rats bred for resistance to the dextran anaphylactoid reaction exhibit contact sensitivity to oxazolone even better than rats which respond to clinical dextran.

Anaphylaxis↗
PubMed1982

Effects of levamisole and D-penicillamine on leucocyte migration into sponge exudates in rats.

Locally administered levamisole and copper levamisole enhanced leucocyte migration into inert sponges implanted into rats for either 4 or 48 h. The stimulated cell was the polymorphonuclear neutrophil. Penicillamine and its copper complex were ineffective. However, all four compounds were effective in enhancing leucocyte migration into sponges implanted into arthritic rats when the drugs were incorporated into the sponges before implantation. Their overall antirheumatic actions may thus have common elements.

Animals↗
PubMed1982

Enhancement of the anaphylactoid reaction in rats by salicylates.

Low doses of sodium or copper salicylate, administered at the same time as agents producing the anaphylactoid reaction in rats, significantly enhanced the onset, height and duration of the responses. The enhancement occurred after intraperitoneal or local administration. Enhanced transport of the high molecular weight agents into the bloodstream is suggested. However, the salicylates did not enhance histamine release from isolated peritoneal mast cells of rats induced by dextran and phosphatidyl serine.

Adjuvants, Immunologic↗
PubMed1982

A possible link between the ability of rat isolated peritoneal mast cells to release histamine when challenged with dextran and the proteins in their plasma membranes.

The plasma membranes of peritoneal mast cells from rats specifically bred for resistance to the dextran anaphylactoid reaction contain a polypeptide of molecular weight about 74,000 daltons which is deficient in those from rats which show the reaction. It is suggested that this polypeptide modifies the dextran receptor in the resistant rats so that histamine release cannot be induced when their mast cells are challenged with dextran.

Animals↗
PubMed1982

Ethylenediamine tetraacetic acid and histamine release from rat mast cells.

The action of ethylenediamine tetraacetic acid (EDTA) on the release of histamine induced by clinical dextran, concanavalin A and compound 48/80 has been studied in rats after intraperitoneal and intrapedial injection as well as in tubes containing isolated peritoneal mast cells. Whereas large doses of EDTA were required for inhibiting histamine release in the whole animal, relatively much smaller concentrations were necessary when the inhibitor was injected locally into the paw or included in the incubation mixture with isolated cells. When dextran was used as the histamine releaser, EDTA was relatively much more effective an inhibitor in vitro than in vivo.

Animals↗
PubMed1982

Delayed hypersensitivity reactions in rats and their response to clinical dextran.

Four colonies of rats were tested for their ability to produce adjuvant-induced arthritis, oxazolone contact hypersensitivity and the dextran anaphylactoid reaction. Tuck Wistar and Hooded Lister rats, both of which respond to dextran, showed disseminated inflammatory lesions after adjuvant and exhibited oxazolone sensitisation, regardless of the age of the animal. Spontaneously hypertensive rats, which at all ages respond to dextran, also responded to adjuvant and oxazolone but only when they were young; as they grew older, this response to these two agents diminished. Wistar NELP rats, which at all ages do not respond to dextran, responded to oxazolone; sensitivity to adjuvant, however, was maximal only in young animals. The link between the ability of rats to resist the dextran anaphylactoid reaction and their failure to respond to adjuvant with disseminated inflammatory lesions has not been confirmed.

Anaphylaxis↗