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Biomedical subjects

A H Briggs

Publications and source records attributed to A H Briggs.

At least 37 records · Page 2Linked to original sources
PubMed1985

Methionine enkephalin as a possible neuromodulator of regional cerebral blood flow.

In swine, cerebral blood flow was documented by a left ventricular injection of radiolabeled 15-micron spheres. Utilizing this procedure, the effect of the putative neurotransmitter methionine-enkephalin on regional cerebral blood flow was systemically evaluated. Our results revealed that a peripheral infusion of methionine enkephalin into miniature swine significantly increased cerebral blood flow in the basal ganglia, cerebellum, pons, inferior parietal cortex and frontal cortex. Non-significant increases were observed in the hippocampus, occipital cortex and medulla oblongata while no effect on blood flow was observed in the pituitary gland. Significance of these results in the potential role of methionine enkephalin as a modulator of blood flow to the brain.

Animals↗
PubMed1984

Supersensitivity to norepinephrine induced by prenatal exposure to ethanol.

Pregnant random bred mice were treated with ethanol (ETOH) (0.33 g/kg) for 1 or 2 days prior to parturition. When compared to saline controls, ETOH-treated adult males had vasa deferentia that were supersensitive to norepinephrine (NE). Tissues from mice prenatally treated for 1 day with ETOH showed a decreased response to electrical stimulation whereas vas deferens obtained from 2-day-treated ethanol showed no significant difference in the response compared to that of controls. These findings indicate that prenatal exposure to ETOH can influence the subsequent sensitivity of the vas deferens to adrenergic stimulation. These changes appear to reflect effects of ETOH during critical periods.

Animals↗
PubMed1983

Ethanol acceptance as a function of genotype amounts of brain [Met]enkephalin.

Our results indicate a negative correlation between the amount of ethanol (10%) consumed and endogenous levels of brain [Met]enkephalin in C57BL/6J (alcohol-preferring) and DBA/2J (alcohol-nonpreferring) inbred mice strains. Additionally, it was found that 8 wk after 1-day starved groups of both C57BL/6J and DBA/2J mice were challenged with ethanol (10%) for 1-day acceptance, they had significantly lower levels of brain [Met]enkephalin compared with their nonalcohol-treated controls. These results suggest that the brain endogenous peptidyl opiates may play a crucial role in alcohol-seeking behavior.

Alcoholism↗
PubMed1982

Whole brain methionine-enkephalin of ethanol-avoiding and ethanol-preferring c57BL mice.

These experiments systematically investigated ethanol preference in both the C57Bl/6N and C57Bl/6J mice utilizing three-choice 2-bottle preference test. In addition, these sublines were evaluated for whole brain methionine-enkephalin levels, which were significantly lower in C57Bl/6J mice (alcohol preferring) compared to C57Bl/6N mice (alcohol non-preferring). This finding supports the involvement of the peptidyl opiates in ethanol seeking behavior.

Alcohol Drinking↗
PubMed1982

Reduced leucine-enkephalin--like immunoreactive substance in hamster basal ganglia after long-term ethanol exposure.

Golden Syrian hamsters were placed individually in cages with three drinking bottles--one empty, one containing water, and the third containing water and ethanol. Control hamsters received water only. After 1 year the experimental hamsters showed a significantly lower concentration of leucine-enkephalin-like immunoreactive substance in the basal ganglia than the control hamsters. This finding indicates that the action of ethanol involves endogenous peptidyl opiates.

Animals↗
PubMed1982

Ethanol intoxication as a function of genotype dependent responses in three inbred mice strains.

Three strains of mice, ICR Swiss, DBA/2J and C57Bl/6J were compared for initial sensitivity, recovery from intoxication, and acute tolerance development to ethanol. The The C57Bl/6J mice were found to be less sensitive and to recover more rapidly from the effects of the same dose of ethanol than the other two strains treated. None of the strains tested demonstrated acute tolerance to ethanol when given the same dose 3 hours later.

Alcoholism↗
PubMed1981

A rapid method of evaluate acute ethanol intoxication in mice.

A simple technique for the evaluation of ethanol intoxication based on the ability of mice to remain on a bar suspended above an electrified grid is reported. The characteristics that make this model useful to measure ethanol induced intoxication include: (a) low variability; (b) high sensitivity; (c) rapidity; (d) requires no previous training of animals to be tested; (e) objective scoring which can be quantified; and (f) dose-dependent correlation between brain and blood ethanol levels and bar holding response.

Alcoholic Intoxication↗
PubMed1979

Single-dose fasting bioequivalence assessment of erythromycin stearate tablets in man.

The bioequivalence of film-coated erythromycin stearate tablets produced by five different manufacturers was evaluated in a balanced incomplete block design involving the five formulations given to 30 fasted subjects over a 3-week study period. Serum levels of erythromycin activity were determined microbiologically. Statistical analysis of variance was performed on the observed bioavailability parameters: maximum serum concentration (Cmax), time to maximum serum concentration (Tmax), and area under the serum concentration-time curve (AUC). There was no statistical difference between formulations for the Tmax parameter. Formulation differences were found, however, based on the analysis of variance of the Cmax and AUC parameters. Two products, although not significantly different from one another, showed significantly greater Cmax and AUC values than the other three products.

Adult↗
PubMed1978

Interaction of hydralazine with tension development and mechanisms of calcium accumulation in K+-stimulated rabbit aortic strips.

A study was made of the effects of hydralazine on K+ contractures in rabbit aortic strips. Measurements were made of effects on tension generation, Ca++ accumulation measured using 45Ca++ (lanthanum method) and 45Ca++ efflux. Hydralazine relaxed established K+ contractures and inhibited tension development when tissue exposure to hydralazine preceded K+ depolarization. Both the threshold and the maximum tension responses of strips to Ca++ (K+-depolarized tissues) were altered by hydralazine in a dose-dependent manner. The Ca++ uptake associated with K+ depolarization was inhibited by relaxant doses of hydralazine; however, hydralazine did not significantly affect the rate of 45Ca++ efflux. Hydralazine also raised the threshold to the inhibitory (relaxant) effects of higher (greater than 2.5 mM) bath concentrations of Ca++. It is suggested that hydralazine inhibits K+ contractures in aortic strips by interference with the entry of Ca++ into the cell, reflecting an effect of hydralazine at the cell surface membrane.

Aorta, Thoracic↗