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Biomedical subjects

N B Thoa

Publications and source records attributed to N B Thoa.

At least 37 records · Page 2Linked to original sources
PubMed1976

Inhibition by cyclopropane of release od norepinephrine, but not dopamine-beta-hydroxylase, from the guinea-pig vas deferens.

Like halothane, cyclopropane reduces stimulation-induced release of norepinephrine, but not release of dopamine-beta-hydroxylase, from the isolated guinea-pig vas deverens. The dissociation between transmitter release and enzyme release in the presence of cyclopropane may be the result of either an increase in the affinity of norepinephrine for binding sites on the vesicular membrane produced by cyclopropane, or a direct effect of cyclopropane on a mechanism of release of norepinephrine that could be controlled independently of release of dopamine-beta-hydroxylase.

Animals↗
PubMed1976

Attack-induced changes in response to decapitation of plasma catecholamines of victim mice.

Male mice of 3 different strains (NIH, C57BR/cdJ and A/HeJ) were exposed individuality (victims) to attack by trained fighter Swiss Webster mice for 10 minutes daily for various numbers of days. Immediately after the last attack the victim mice were decapitated along with unattacked control mice of the appropriate strain, and plasma norepinephrine (NE) and epinephrine (E) were measured. The concentration of NE was significantly lower in decapitated C57BR/cdJ mice than in the other 2 strains. The concentrations of E and NE in the plasma of decapitated C57BR/cdJ and A/HeJ mice were significantly greater after 4 days of attacks, whereas in NIH mice plasma levels of only NE were greater and this occurred only after 14 days of attacks. After 7 days of exposure to attack, C57BR/cdJ and A/HeJ victim mice were permitted to rest for various periods of time. In C57BR/cdJ animals plasma E returned to almost normal levels after 2 days, and NE after 4 days, while in A/HeJ mice plasma E and NE returned to control levels already after 1 day of rest.

Adrenal Glands↗
PubMed1975

Inhibition by halothane of release of norepinephrine, but not of dopamine-beta-hydroxylase, from guinea-pig vas deferens.

Halothane strikingly decreases spontaneous and electrically stimulated release of norepinephrine from the isolated guinea pig hypogastric nerve--vas deferens preparation. This depression of adrenergic discharge appears to be a direct action on the sympathetic nerve endings and may in part account for the cardiovascular depression seen during halothane administration. Although halothane depressed stimulation-induced release of norepinephrine, it did not proportionately diminish release of dopamine-beta-hydroxylase. Possible mechanisms of the dissociation between catecholamine and enzyme release are discussed.

Animals↗
PubMed1975

Modification of morphine-withdrawal syndrome in rats following transauricular electrostimulation: an experimental paradigm for auricular electroacupuncture.

The experimental paradigm reported here provides a useful animal model with which to further study the effects of regional electrostimulation and its possible relationship with electrical acupuncture. What similarities there may be between electrical acupuncture and the technique of regional electrocerebral stimulation used for production of electrosleep and electronarcosis in animals and man (Wageneder et al., 1966) remain to be elucidated. Further research studies, both clinical and basic, are clearly needed to answer some of the questions relating to the safety, efficacy, and possible mechanisms by which a technique such as electrical acupuncture may exert its effects.

Acupuncture Therapy↗
PubMed1973

Effects of vinblastine on catecholamine-biosynthetic enzymes in heart, sympathetic ganglion and adrenal glands of rats.

1. The effect of vinblastine on the activities of dopamine-beta-hydroxylase (DBH) in heart, superior cervical ganglion and adrenal glands of rats and tyrosine hydroxylase (TH) and phenylethanolamine-N-methyl transferase (PNMT) in adrenal glands was examined.2. In the superior cervical ganglion and heart, DBH activity decreased within hours, reached a minimum in 3 to 5 days and slowly returned towards normal over the next 2 weeks.3. There was an increase in the activities of TH, DBH and PNMT in adrenal glands which was prevented by adrenal denervation.4. When the same total dose of vinblastine was administered subdivided over a period of 5 days, enzyme activities in heart, superior cervical ganglion or adrenal glands remained unchanged.

Adrenal Glands↗