Mass spectrometry of derivatives of cyclopropene fatty acids.
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Diketo fatty acids prepared by ozonization of cyclopropene fatty acids have been separated and purified by chromatographic techniques. Mass spectra of esters of these compounds and of methanethiol adducts of cyclopropene acid esters are reported and interpreted. Location of the ring from examination of mass spectra of these derivatives appears to be a straightforward matter. (+info)
Release of endogenous noradrenaline from an isolated muscular artery. Release of endogenous noradrenaline from an isolated muscular artery.
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1. The release of noradrenaline by field stimulation of vasoconstrictor nerves has been studied in isolated preparations of the main uterine artery of the guinea-pig.2. In preparations from virgin animals stimulation with trains of 3000 square pulses at 5 and 25 pulses/sec resulted in mean overflows of 0.56 ng/g.pulse and 1.53 ng/g.pulse respectively.3. Inhibition of monoamine oxidase and catechol-O-methyltransferase had no consistent effect on overflow at either stimulation frequency.4. Desmethylimipramine (10(-5)M) caused, on the average, a 2.4-fold increase in overflow following stimulation at 5 pulses/sec while phenoxybenzamine (10(-5)M) caused a 3.8-fold increase. Neither of these drugs caused a significant alteration of the overflow during stimulation at 25 pulses/sec.5. Treatment of the tissues with desmethylimipramine plus normetanephrine (4.5 x 10(-4)M) caused no more increase in overflow than treatment with desmethylimipramine alone.6. It is concluded that enzymatic metabolism of noradrenaline at the synapse is of little functional importance in this tissue, and that the most important mechanism of transmitter inactivation is by nervous re-uptake. Although phenoxybenzamine was more effective than desmethylimipramine in increasing transmitter overflow, no evidence was obtained to support the view that this effectiveness was due partly to blockade of ;Uptake 2'.7. There was sometimes very low overflow of noradrenaline from arteries taken from animals in the last week of pregnancy. In these instances overflow following stimulation at 5 pulses/sec was not increased by phenoxybenzamine treatment of the tissue.8. Methylene blue and fluorescence microscopic techniques indicated that the terminal adrenergic axons in each artery possess approximately 8.74 x 10(5) varicosities. The mean tissue content of noradrenaline was found to be 9.6 mug/g or 29 ng/artery. These results have been correlated with known morphological and electrophysiological data to derive a peak post-junctional concentration of noradrenaline during transmission of about 4 x 10(-4)M.9. The fraction of total noradrenaline content of the artery released per pulse (under the influence of phenoxybenzamine) had a mean value of 2.2 x 10(-4). (+info)
Evaluation of mechanisms controlling the release and inactivation of the adrenergic transmitter in the rabbit portal vein and vas deferens.
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1. A method is described for the detection and assay of picogramme quantities of noradrenaline. This involves transferring Krebs solution containing noradrenaline to a cascade system where the catecholamine may be bioassayed on superfused preparations of the rabbit aorta and iliac artery.2. Electrical field stimulation of the rabbit vas deferens and portal vein caused the release, into the bathing medium, of a material which was identified by pharmacological and chemical tests as noradrenaline.3. Cocaine (0.3-5 mug/ml) caused a marked increase in noradrenaline output after electrical stimulation of the portal vein and vas deferens. This effect appeared to be maximal at a concentration of 2.4 mug/ml; when the cocaine concentration was increased above 10 mug/ml the noradrenaline output was greatly reduced.4. Phenoxybenzamine (5 mug/ml) caused a 4-8 times greater increase in noradrenaline output than cocaine; however, the increase in output due to phenoxybenzamine was much smaller in tissues pretreated with cocaine.5. Corticosterone (20 mug/ml) increased noradrenaline output by 30-40% in untreated vas deferentia, but caused a 300% increase in output in tissues pretreated with cocaine. Cocaine also caused a much greater increase in output in tissues pretreated with corticosterone than in untreated tissues.6. Treatment with pargyline plus tropolone caused a 100-200% increase in noradrenaline output; this effect was not modified by cocaine, but was abolished when the tissues were pretreated with either phenoxybenzamine or corticosterone.7. When tissues were stimulated for 240 pulses at 1-16 Hz, the output per pulse of noradrenaline increased linearly with the logarithm of the frequency of stimulation. This relationship between frequency and output was seen in both untreated tissues, and in tissues treated with cocaine, phenoxybenzamine, corticosterone or pargyline plus tropolone.8. It is concluded that cocaine enhances output by blocking the neuronal reuptake of noradrenaline, and corticosterone by blocking the extraneuronal uptake and subsequent metabolism of noradrenaline. Phenoxybenzamine acts by blocking both neuronal and extraneuronal uptake mechanisms. There appears to be a dynamic balance in the distribution of noradrenaline between the two uptake mechanisms after the release of the transmission from the nerve endings.9. It is calculated that more than 90% of the noradrenaline released by nerve stimulation (240 pulses at 2-16 Hz) is inactivated by neuronal and extra neuronal uptake mechanisms.10. It is calculated that the fraction of the total noradrenaline store that is released by one pulse at 2 Hz is 6.6 x 10(-5) in the portal vein and 5.6 x 10(-5) in the vas deferens; the corresponding values at 16 Hz were 15.9 x 10(-5) and 16.2 x 10(-5). (+info)
In vitro antiviral activity and preliminary clinical trials of a new adamantane compound.
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A compound, 1'-methyl spiro (adamantane-2,3'-pyrrolidine) maleate, chemically related to the antiviral drug amantadine, was tested for activity in vitro against a number of human respiratory viruses. By a variety of techniques, it was shown to be active against a wide range of human and animal influenza A viruses. The effect was, however, variable and ranged from high activity against two 1957 Asian strains to no observable activity against a 1971 strain. Like amantadine, the drug did not inhibit the growth of influenza B viruses. It was also inactive against a number of paramyxoviruses. Unlike amantadine, the drug did inhibit rhinoviruses, but to a lesser extent than myxoviruses. The coronavirus 229E was also sensitive to the action of the drug in vitro. Although an earlier trial in volunteers showed that, when given orally from 2 days before until 5 days after virus challenge, the drug was protective against infection with influenza A/Hong Kong/68 virus, a similar trial in volunteers challenged with rhinoviruses 2 and 9 revealed no useful activity against rhinoviruses in man. (+info)
Cyclitol glucosides and their role in the synthesis of a glucan from uridine diphosphate glucose in Phaseolus aureus. Characterization of some cyclitol glucosides and their synthesis.
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Short-chained sugar compounds, thought to be involved in the synthesis of callose, were formed in small amounts from UDP-glucose by soluble extracts from hypocotyls of seedlings of Phaseolus aureus. The properties of the glycosides were investigated by treatment with various chemicals and analysis by paper chromatography, g.l.c. and mass spectrometry. The data obtained support the characterization of these compounds as myoinositol-beta-glucoside and diglucosylmyoinositol. The cyclitol moiety was provided by the enzyme extract. Free myoinositol was not the immediate substrate but a compound containing myoinositol, isolated from the enzyme extract, may be involved. The method of synthesis of these glucosides is compared with that of other cyclitol glycosides. (+info)
Tropism of Mycoplasma gallisepticum for arterial walls.
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The fatal encephalopathy associated with M. gallisepticum strain S6 in turkey poults was completely curable by treatment with tylosin or pleuromutilin. The lesions of cerebral polyarteritis disappeared after therapy. Polyarthritis developed in some birds after recovery from encephalitis. Immunofluorescent studies revealed that intravenously injected organisms became localized as microcolonies within the walls of cerebral and periarticular arteries, and in the glomeruli. Turkey IgG deposition was demonstrated on the glomerular basement membranes, but not in the arterial lesions. The results suggest that the pathologic changes caused by this microorganism are due to selective localization and growth in arteries. (+info)
Microbial degradation and assimilation of n-alkyl-substituted cycloparaffins.
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Studies were conducted on the oxidation and assimilation of n-alkyl-substituted cycloalkane substrates by several hydrocarbon-utilizing microorganisms. These microorganisms utilized heptadecylcyclohexane and dodecylcyclohexane as the sole source of carbon and energy. Neither methylcyclohexane nor ethylcyclohexane was utilized as a growth substrate by any organisms tested. Gas-liquid chromatographic analyses of fatty acids present in cells after growth on dodecylcyclohexane confirm direct incorporation of both alpha- and beta-oxidation products. Growth patterns of these organisms on n-alkyl-substituted cyclohexane fatty acids of varying chain lengths suggest a greater probability of ring cleavage when the side chain contains an odd number of carbons. (+info)
Rimantadine therapy of influenza A infection in mice.
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Eighty per cent of mice infected with a mouse-adapted strain of influenza virus died within 3 to 8 days after infection. Rimantadine given at maximum protective doses reduced mortality to 10%. This protection is dose related and can be demonstrated with doses from 4.5 to 24 mg per kg per day. Significant survival rates are shown by delaying treatment as long as 48 hr after infection. Lungs of treated mice have significantly less virus than those of controls at 24, 48, and 72 hr after infection. Antibody production as measured by hemagglutination inhibition is not different in treated and controlled mice. These results indicate that rimantadine is an effective prophylactic and therapeutic agent and that its activity is associated with decreased viral titers. (+info)