PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Pyrogallol”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1978

Effect of dissolved oxygen levels on oxidative degradation of pyrogallol.

Pyrogallol decomposition in aqueous systems with various dissolved oxygen levels was studied. The reduced dissolved oxygen levels were produced by deaeration via gas permeation. Dissolved oxygen levels were determined using a dropping mercury electrode polarograph. Degradation rates, T90, and relative protection indexes are discussed. Even at dissolved oxygen levels of less than 0.05 ppm, some decomposition of pyrogallol occurred, indicating nonoxidative pathways or the necessity of total removal of dissolved oxygen to afford complete protection. Apparently, reducing the level of dissolved oxygen is a viable alternative to stabilization of aqueous pyrogallol solutions, since the T90 was increased from 1.9 days in water with dissolved oxygen levels of 9.05 ppm to 114.4 days in water with dissolved oxygen levels of less than 0.05 ppm.

Drug Stability↗
PubMed1979

[Influence of desoxycorticosterone on the reaction of isolated segments of coronary arteries to noradrenaline in the presence of pyrogallol].

The effect of the desoxycorticosterone on the noradrenaline-induced relaxation of coronary arteries waw studied in vitro, after a known inhibitor of COMT, pyrogallol. Relaxation induced by noradrenaline was enhanced by desoxycorticosterone. Relaxation in response to noradrenaline was increased by desoxycorticosterone. Pyrogallol potentiated the responses of coronary strips to noradrenaline and also reduced or abolished the enhancing effects of desoxycorticosterone. It is concluded that desoxycorticosterone enhances the reponse of coronary smooth muscle to noradrenaline by inhibiting and enzymatic pathway for the inactivation of catecolamines.

Animals↗
PubMed1978

[Influence of pyridoxal-5'-phosphate on the responses of isolated coronary arteries to adrenaline, in the presense of pyrogallol].

The effect of PLP on the adrenaline-induced relaxation of coronary arteries was studied in vitro, after known inhibitor of COMT, Pyrogallol. Relaxation of response to adrenaline were increased by PLP. Pyrogallol potentiated responses of coronary strips to adrenaline and also reduced or abolished the enhancing effects of PLP. It is concluded that PLP enhances the response of coronary smooth muscle to adrenaline by inhibiting a enzymatic pathway for the inactivation of catecholamines.

Animals↗
PubMed1978

[Influence of pyridoxal-5'-phosphate on responses of isolated coronary arteries to noradrenaline, in the presence of pyrogallol].

The effect of PLP on the noradrenaline-induced relaxation of coronary arteries was studied in vitro, after known inhibitor of COMT, Pyrogallol. Relaxation of response to noradrenaline were increased by PLP. Pyrogallol potentiated responses of coronary strips to noradrenaline and also reduced or abolished the enhancing effects of PLP. It is concluded that PLP enhances the response of coronary smooth muscle to noradrenaline by inhibiting a enzymatic pathway for the inactivation of catecolamines.

Animals↗
PubMed1979

Mutagenic and colicine-inducing activity of two antioxidants: pyrogallol and purpurogallin.

The antioxidants pyrogallol and its oxidative derivative, purpurogallin, both induce colicine E2 as well as base substitution and frameshift mutations. Because of the bactericidal effect of purpurogallin, its mutagenicity could be best demonstrated by short-term exposure followed by dilution on the test plates. The colicine-inducing potential of purpurogallin was also observed when tested directly on the plates.

Aminoacridines↗
PubMed1977

Influence of Steroidal enzyme inducers on the toxicity of pyrogallol, pargyline and nialamide.

In rats, the toxic manifestations of overdosage with with parcyline (a monoamine oxidase inhibitor) or pyrogallol (a catechol-o-methyltransferase inhibitor) were diminished by treatment with the more potent steroidal (pregnenolone-16alpha-carbonitrile, spironolactone, etc.) or nonsteroidal (phenobarbital) catatoxic substances. Except for significant protection offered by glucocorticoids (triamcinolene, prednisolone acetate) against pargyline, all other pretreatments (progesterone, estradiol, desoxycorticosterone acetate, etc.) either had no influence on or increase the deleterious effects of the two amine inhibitors. Nialamide intoxication was exacerbated by most of these conditioners.

Animals↗
PubMed1978

The potentiating effect of clorgyline and pyrogallol on the blood pressure responses to norepinephrine.

Intraventricular administration of norepinephrine (NE) into pentobarbital anesthetized rats elicits a pressor or a depressor effect depending on the dose injected: after a low dose, a depressor response is seen while after a high dose, a pressor response is observed. In the animal pretreated intraventricularly with clorgyline or pyrogallol, the hypotensive effect of a low dose of NE was reversed to a hypertensive effect, while the hypertensive effect of a high dose of NE was markedly potentiated. This result suggests that brain monoamine oxidase and catechol-o-methyltransferase can metabolize centrally released NE before it leaks into the peripheral circulation.

Animals↗
PubMed1976

Studies on the effects of pyrogallol and the structurally related dopa decarboxylase inhibitor RO4-4602 on acetaldehyde metabolism.

Microanalytic procedures for the determination of AcH in whole blood from EtOH-intoxicated animals given PG or related drugs should utilize a hemolysis step in 0.5 N PCA in order to inhibit PG-dependent AcH production in vitro. Thiourea may also be included as an added protective measure. RO4-4602, a clinically important drug that contains a PG ring structure, is a moderate in vitro inhibitor of AldDH activity, comparable in potency to PG, chloral hydrate, or diethyldithiocarbamate.

Acetaldehyde↗
PubMed1978

The influence of an extraneuronal compartment on the relaxation of the cat nictitating membrane in vivo.

1 Contractions of the cat nictitating membrane were elicited on stimulation of the internal carotid nerve, and the effects were studied of desipramine and two inhibitors of catechol-O-methyltransferase, U-0521 and pyrogallol, on the subsequent relaxation of the muscle. 2 The relaxation of the nictitating membrane occurred in at least two phases. The late phase of relaxation was prolonged after increase in the period of nerve stimulation and the duration of this phase was further prolonged after treatment with pyrogallol. 3 After inhibition of neuronal uptake of noradrenaline with desipramine both the early and late phases of relaxation were increased in duration, and subsequent administration of pyrogallol or U-0521 caused a further increase in the duration of the late phase of relaxation. 4 The results suggest that the late phase of relaxation of the nictitating membrane is influenced by efflux of noradrenaline from an extraneuronal pool.

Animals↗