Further studies on the histidine‐histamine relationship <i>in vivo</i>: effects of endotoxin and of histidine decarboxylase inhibitors

Reilly, Margaret A.; Schayer, Richard W.

doi:10.1111/j.1476-5381.1968.tb08484.x

Cited by 34 publications

(12 citation statements)

References 19 publications

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“…Animals were sacrificed post-14C-L-histidine at 5 minutes in stomach experiments, and 3 days in skin experiments; the 3 day interval was to permit dissipation of loosely bound a4C-histamine so that mast cell 14C-histamine of skin was measured. These intervals are in accordance with our previous tests [5]. For brain tests, animals were sacrificed 25-40 minutes posthistidine unless a shorter interval was required by experimental conditions (exp.…”

Section: Animal Experimentationmentioning

confidence: 91%

“…However, when decaborane-treated mice were injected with 14C-L-histidine, stomach 14C-histamine content was significantly higher than for controls [10]. A similar in vivo test was made on rats; ~-HH, a strong inhibitor of histidine decarboxylase [5] was also tested. Two groups of rats, 111 g average weight, were injected with vegetable oil, and one group with decarborane 1.5 mg in oil; all were fasted for the duration of the experiment.…”

Section: Stomach Experiments Experiments 9 Decaborane Inhibits Hisfidinementioning

confidence: 93%

“…For brain and stomach the 14C-histamine concentration is expressed as dpm per thousand dpm total 14C; this unit was used to eliminate the possibility that a drug might reduce 14C-histamine by reducing the availability of substrate, 14C-L-histidine. In short-term experiments, total ~4C is closely proportional to the z4C-L-histidine concentration [5,6]. For skin, because of the 3 day interval between injection of ~4C-L-histidine and sacrifice, total ~4C values were low and of no relevance; therefore ~4C-histamine is expressed as dpm per gram skin.…”

Section: Animal Experimentationmentioning

confidence: 99%

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Effect of histidine decarboxylase inhibitors and other drugs on histamine formation in vivo

Schayer

Reilly

1974

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A number of compounds alleged to inhibit histidine decarboxylase in vitro and in vivo, were tested in mice for ability to reduce histamine formation in cell types containing this enzyme. Mice were pretreated with 'inhibitor' or saline, injected with 14C-L-histidine, and after an interval suitable for each cell type, sacrificed. For mast cell histidine decarboxylase, skin was assayed; for enzyme in enteroehromaflin-like cells, stomach was assayed; for brain ceils (cell type unidentified at present) whole brain was assayed. Most tested compounds had little or no effect on histamine formation. Only one drug, 4-imidazole-3-amino-2-butanone showed strong activity in both skin and stomach samples; it did not affect brain histamine formation, possibly because it does not enter brain.

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Section: Animal Experimentationmentioning

confidence: 91%

Section: Stomach Experiments Experiments 9 Decaborane Inhibits Hisfidinementioning

confidence: 93%

Section: Animal Experimentationmentioning

confidence: 99%

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Effect of histidine decarboxylase inhibitors and other drugs on histamine formation in vivo

Schayer

Reilly

1974

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“…This is a view originally suggested by Schayer (1960a, b). It is perhaps unlikely that the increased tissue histamine levels are the result of a reduced ability to destroy histamine since it has been reported that endotoxin has no effect on diamine oxidase activity or on histamine methylation (Reilly & Schayer, 1968;1970).…”

Section: The Role Of Histamine In Endotoxin Shockmentioning

confidence: 99%

Feline endotoxin shock: effects on tissue histamine and histidine decarboxylase activity

Parratt

Saleh

Waton

1986

British J Pharmacology

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Tissue histamine levels as well as specific and non‐specific histidine decarboxylase were examined before and at various times (5 and 10 min) after the intravenous injection of a lethal dose (2 mg kg−1) of E. coli endotoxin in anaesthetized cats. Histamine levels were increased 5 min after endotoxin, especially in the skin, liver, lung and stomach. There was evidence, in most of the cats, for a rapid and substantial activation of specific histidine decarboxylase especially in the lungs, liver, heart and gastrointestinal tract 5–10 min after endotoxin administration. It is suggested that endotoxin induces the local formation of histamine and that this formation and local release may contribute to the pathophysiology of endotoxin shock in this species.

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“…With improved means for investigating histamine formation and catabolism in vivo (Reilly & Schayer, 1968a, 1968b, 1970, 1971a, 1971b we have extended studies to mice.…”

Section: Introductionmentioning

confidence: 99%

Effect of glucocorticoids on histamine metabolism in mice

Reilly

Schayer

1972

British J Pharmacology

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Summary1. Histamine formation and catabolism were studied in vivo in standardized experiments; for the former, animals pretreated with inhibitors of histamine catabolism were killed 10 min after intravenous injection of "C-L-histidine; for the latter, no inhibitors were used and animals were killed 2 5 min after intravenous injection of "IC-histamine. In vitro assays of histidine decarboxylase activity were also made. 2. Pretreatment of adrenalectomized mice with cortisol for one day caused a major alteration in histamine formation; stomach and intestine were abnormally high in the "IC-histamine: total "IC ratio, while most other tested tissues were lower. Brain and thymus were unaffected. Cortisol treatment caused a marked increase in urinary excretion of both "C-histamine and total "C. 3. Following injection of a rapidly absorbed corticoid, significant effects on urine and stomach were demonstrable at 30 min and 4 h, respectively. 4. In cortisol-treated adrenalectomized mice histidine decarboxylase activity, relative to controls, was decreased in lung but virtually unaffected in kidney, heart, muscle and liver. In stomach, activity was increased but the statistical significance was low. 5. In mice injected with "C-histamine, cortisol pretreatment caused a small drop in tissue levels of "C-histamine, "C-methylhistamine and total "IC, but increased levels in urine. In all cases, however, the ratio of the two amines to total "C was not significantly different from controls. 6. From the foregoing experiments it was concluded that the results in (2) could be largely attributed to entry into urine of "C-histamine and total 'C, thus reducing the availability of these substances in blood for extraction by tissues. In stomach, the cortisol-induced increase in histamine formation may involve some process other than increased histidine decarboxylase activity. 7. The activation of histidine decarboxylase in liver and lung of intact mice by Freund's adjuvant, or by endotoxin, was reduced by corticoid treatment. 8. In a single short experiment on the effect of cortisol on histamine formation in adrenalectomized rats, results from stomach, lung and heart, the only tissues assayed, were slimilar to those from the mouse experiment.

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Further studies on the histidine‐histamine relationship in vivo: effects of endotoxin and of histidine decarboxylase inhibitors

Cited by 34 publications

References 19 publications

Effect of histidine decarboxylase inhibitors and other drugs on histamine formation in vivo

Effect of histidine decarboxylase inhibitors and other drugs on histamine formation in vivo

Feline endotoxin shock: effects on tissue histamine and histidine decarboxylase activity

Effect of glucocorticoids on histamine metabolism in mice

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