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Biomedical subjects

R W Schayer

Publications and source records attributed to R W Schayer.

At least 19 recordsLinked to original sources
PubMed1982

The histamine-induced skin reaction in schizophrenic and normal subjects.

Most published data on histamine skin tests on schizophrenic patients show them to be insensitive relative to normals or other psychotic patients. However, experimental conditions have varied and in most cases only a single dose of histamine was used. We have compared 13 volunteer controls and 16 paranoid schizophrenics; each subject was injected intradermally with histamine, 10, 20, and 50 microgram, doses predetermined in volunteers to give a dose-response curve. Wheal and flare were measured at 10 and 20 minutes, intervals near the time of maximum flare. We found no statistically significant differences between normal controls and schizophrenic patients.

Adult↗
PubMed1981

Involvement of diamine oxidase in catabolism of 14C-putrescine in mice in vivo with special reference to the formation of gamma-aminobutyric acid.

Tissues of mice killed 2.5 or 30 min after injection of 14C-putrescine, contained 14C-gamma-aminobutyric acid, an unidentified 14C-compound, and unchanged 14C-putrescine. In mice pretreated with aminoguanidine, a powerful inhibitor of diamine oxidase, and then with 14C-putrescine, tissue levels of the radioactive catabolites, gamma-aminobutyric acid and the unidentified compound were markedly reduced. The data suggest that diamine oxidase is involved in the first step of putrescine metabolism and that intestine is the main site for this step. This and other aspects of putrescine metabolism are discussed.

Amine Oxidase (Copper-Containing)↗
PubMed1978

Effect of histamine methylation inhibitors on entry of 14C-histamine into brain.

Pretreatment of mice, rats and guinea pigs with inhibitors of histamine methylation, followed by systemic injection of 14C-histamine, results in a significant increase in brain 14C-histamine relative to controls. It is suggested that the histamine methylating enzyme participates in the blood-brain barrier to histamine.

Amodiaquine↗
PubMed1978

Effects of various S-adenosylmethionine preparations on histamine methylation in vitro and in vivo.

To test possible enhancement of in vivo methylation of histamine, mice were injected with S-adenosylmethionine (SAM) of approximately 96% purity. Instead of the expected enhancement, very strong inhibition of methylation was observed. Tests indicated that S-adenosylhomocysteine (SAH) probably was not the inhibitor. Pure SAM, from another source, showed no inhibition of methylation in rats and guinea pigs, and only slight inhibition in mice. Pure SAM was much more effective than the 96% SAM for histamine methylation in vitro. It seems either that injected SAM cannot enter cells containing the histamine methylating enzyme (HME), or that the endogenous supply of SAM is optimal. The inhibitor may be structurally related to SAM, possibly a by-product of SAM synthesis. As it is very effective even in the presence of large amounts of SAM, in pure form it would probably be the most potent inhibitor of histamine methylation available.

Animals↗
PubMed1975

Methyl derivatives of histamine; interaction with histamine metabolism.

Several histamine analogs, with ring or side chain methyl groups, were tested for interaction with certain aspects of 14C-histamine metabolism. The physiological catabolite, denoted as 3-methylhistamine under the nomenclature we have adopted, is known to inhibit histamine methylation in vitro and in vivo. At low concentrations, all analogs inhibited histamine methylation by mouse brain homogenates; however 3-methylhistamine was completely ineffective against the highly active enzyme from rat didney, while 2-methylhistamine was most effective. None of the drugs showed a significant effect on in vivo formation of 14C-histamine by mouse stomach. All analogs had a definite effect on the distribution and fate of intravenously injected 14C-histamine. The 2-methyl analog was the strongest in vivo inhibitor of histamine methylation, and 3-methylhistamine next. The side chain N-methylated histamies altered uptake of 14C-histamine in some tissues but inhibited methylation weakly, if at all. Data on blood kidney and urine for 4-methylhistamine were unique, and suggested some effect on tubular reabsorption. 2-methylhistamine may prove to be the inhibitor of choice for in vivo studies on histamine methylation.

Animals↗
PubMed1975

Activity changes in mouse brain histidine decarboxylase.

Mice were tested for effects of various factors on histidine decarboxylase of whole brain, or major brain regions. Factors included age, sex, fasting and feeding, season of year, time of day, freezing for various time intervals, and intracerebral injection of protein synthesis inhibitors daily for 2-5 days. In the latter test, 5 day treatment with acetoxycycloheximide reduced brain histidine decarboxylase activity. In one experiment, in which a marked activity increase was observed, brain infection seemed to be the stimulus. Brain enzyme activity in normal mice showed large fluctuations over periods of several months to one year; presumably this is of some physiological significance but the causes are obscure.

Age Factors↗
PubMed1975

Comparison of in vitro and in vivo histamine methylation by tissues.

A method for determining the histamine-methylating enzyme (HME) using crude enzyme, and minute quantities of the substrate, was applied to tissues of mice, guinea-pigs and rats. Since high levels of endogenous histamine can affect the results, tissue homogenates were dialyzed prior to incubation. Findings were compared with in vivo data on methylating ability of individual tissues; most of this in vivo data is published but a new test of guinea-pig tissues was made using amodiaquine as an inhibitor. The correlation was good, better than that obtained by other procedures. It was observed that dialysis caused an increase in HME for some guinea-pig tissues, but a loss for some mouse tissues. Possible explanations are considered. Quinacrine N-mustard, a derivative of a known HME inhibitor, was tested in mice; it altered the distribution of injected 14C-histamine but showed no evidence of HME inhibition.

Amodiaquine↗