The effects of acute hypercapnia on cerebral indole amine metabolism

1978 ◽  
Vol 56 (2) ◽  
pp. 223-226 ◽  
Author(s):  
V. MacMillan

The effects of 1-h exposure to hypercapnia ([Formula: see text], 90–110 mmHg) on cerebral indole amine metabolism were studied in rats by measurement of cerebral hemisphere contents of tryptophan, 5-hydroxytryptophan (5-HTP), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA). 5-HIAA content was increased after 1-h exposure to hypercapnia, whereas tryptophan, 5-HTP, and 5-HT remained unchanged from control. The accumulation of 5-HTP after decarboxylase inhibition with 3-hydroxybenzyl hydrazine was increased in hypercapnic rats and indicated an increased activity of tryptophan hydroxylase. During the 1-h exposure to hypercapnia there was increased accumulation of 5-HT after monoamine oxidase inhibition with pargyline and increased accumulation of 5-HIAA arter probenecid. The results indicate an increased synthesis and degradation of indole amines in acute hypercapnia.

1961 ◽  
Vol 107 (447) ◽  
pp. 244-249 ◽  
Author(s):  
W. G. Dewhurst ◽  
C. M. B. Pare

In order to test whether a drug is an inhibitor of monoamine oxidase in the human subject, three main measures are available:1. We can measure an increased excretion of the normal substrates of the enzyme, e.g. tryptamine (Sjoerdsma, et al., 1959b).2. We can measure a decreased excretion of the metabolites resulting from the enzyme's action, e.g. 5-hydroxyindoleacetic acid (5-HIAA).3. We can administer a loading dose of an enzyme substrate and observe how the subject deals with it before and after the drug, e.g. 5-hydroxytryptamine (Sjoerdsma et al., 1958), and epinephrine (N-methyl-C14) (Resnick et al., 1958).


1982 ◽  
Vol 60 (3) ◽  
pp. 308-312
Author(s):  
V. MacMillan

The effects of imidazole-4-acetic acid (IMA, 100–400 mg/kg) on indole amine metabolism were studied by measurement of the cerebral hemisphere and brain stem contents of tryptophan, 5-hydroxytryptophan (5-HTP), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA). The results indicated that IMA does not alter the steady-state contents of brain indole amines. Furthermore, IMA failed to alter the levels of 5-HTP, 5-HT, or 5-HIAA in animals pretreated with 3-hydroxybenzyl hydrazine (a decarboxylase inhibitor), pargyline (a monoamine oxidase inhibitor), or probenecid (a compound which blocks 5-HIAA transport out of brain). These results suggest that altered serotonin metabolism is not a factor in the genesis of the behavioral or electroencephalographic changes produced by IMA.


1989 ◽  
Vol 46 (5) ◽  
pp. 528-536 ◽  
Author(s):  
Rainer Schulz ◽  
Karl-Heinz Antonin ◽  
Edgar Hoffmann ◽  
Maria Jedrychowski ◽  
Eric Nilsson ◽  
...  

2016 ◽  
Vol 14 (2) ◽  
pp. 163-165 ◽  
Author(s):  
Hamlin Emory ◽  
Neptune Mizrahi

We present clinical, electroencephalographic and low-resolution electromagnetic tomography data that support combined treatment with insulin and a monoamine oxidase inhibitor in a patient with type 1 diabetes. We suggest that brain imaging data can identify a subgroup of patients who are likely to benefit from an insulin regimen and monoamine oxidase inhibition to improve glycaemic control, cardiovascular function, normalize the circadian rhythm and restore perception of glycaemic awareness.


2016 ◽  
Vol 41 (9) ◽  
pp. 2173-2178 ◽  
Author(s):  
David S. Goldstein ◽  
Yunden Jinsmaa ◽  
Patti Sullivan ◽  
Courtney Holmes ◽  
Irwin J. Kopin ◽  
...  

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