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Biomedical subjects

T E Reed

Publications and source records attributed to T E Reed.

At least 37 records · Page 2Linked to original sources
PubMed1980

Acute effects of ethanol in vivo on neuromuscular transmission.

The effects in vivo of acute doses of ethanol on impulse transmission in the region of the neuromuscular junction are poorly known. These effects were studied with a new procedure, using mouse tails in a constant temperature chamber to study the delay in nerve-to-muscle impulse transmission. A saline control and five ethanol doses (0.5, 1.0, 1.4, 2.0, 4.24 g/kg) were used with 96 mice. The interval ("residual latency", RL), between (a) the peak of the compound nerve action potential and (b) the first peak of the associated compound muscle action potential, was measured. Ethanol was given IP and tail nerve stimulations were done at 4 min intervals to 16 min post-ethanol. The mean pre-ethanol RL was 0.93 +/- 0.01 (SE) msec; about 25% of this time should be synaptic delay and the remainder is nerve and muscle fiber conduction time. Individual post-ethanol relative RL (RRL) values were calculated for each moue, based on its pre-ethanol value. With doses of 1.0 g/kg and higher there was a mean increase in RRL; at 16 min this increase was 0.8 to 4.4% (all p less than 0.01). At 0.5 g/kg, and also at higher doses, there was a significantly (p less than 0.01) increased variance in RRL 8 to 16 min post-ethanol. A marked correspondence between mean RRL and ataxia is apparent. This appears to be the first in vivo demonstration of acute effects of ethanol on neuromuscular transmission. The methods and mice used may comprise a useful animal model for detecting acute effects of low doses of ethanol on synaptic function.

Animals↗
PubMed1978

Marked individual variability in heart rate "normalization" by ethanol.

In order to test Kissin's (1974) concept of "normalization" by ethanol (deviant prealcohol parameter values becoming less deviant after alcohol) in nonalcoholics, data on unselected mice and nonalcoholic humans were analyzed. These data were on heart rates (HR) of 1055 HS mice and 24 young adults, measured before and after receiving a dose of ethanol (mice: 1.4g/kg, i.p.;humans: 1.3g/kg, oral). Both mice and humans, on the average, show marked "normalization" inintially low HR usually increasing after alcohol, and initially high HR usually decreasing. The correlation between (1) deviation in HR from the prealcohol mean and (2) change in HR after alcohol was -0.803 for mice and -0.538 for humans. There is very great individual variability, however, in the degree of this normalizing response, some individuals normalizing strongly and others not at all. Although first described in alcoholics, strong normalization by alcohol of several psychophysiological parameters is now known to occur in mice and seems likely to occur in some nonalcoholic humans. The possible relevance of these results to predisposition to alcoholism remains to be shown.

Animals↗
PubMed1978

Racial comparisons of alcohol metabolism: background, problems, and results.

The background of and problems in making comparisons among different racial groups in their rates of alcohol metabolism are reviewed. The results of five studies are discussed. It is concluded that the variation among races in rate of alcohol metabolism is not different in kind than variation among individuals within a given race. There are good reasons to expect the former variation to be smaller than the latter.

Alcohol Oxidoreductases↗
PubMed1976

Alcohol and acetaldehyde metabolism in Caucasians, Chinese and Amerinds.

Ethanol (0.4 to 0.8 g/kg in 30 minutes) was given by mouth to 102 healthy young volunteers (37 Caucasian men, 21 Caucasian women, 20 Chinese men and 24 Ojibwa men). Venous blood concentrations of ethanol and acetaldehyde 60, 90, 120 and 150 minutes after the end of drinking were measured by gas chromatography. The calculated rates of ethanol metabolism in the Caucasian men and women did not differ, but the overall group means for subgroups of Caucasians (103.6 mg/kg-h), Chinese (136.6 mg/kg-h) and Ojibwa (182.7 mg/kg-h) with decreasing postabsorption values differed significantly from each other. Mean acetaldehyde values paralleled the rates of ethanol metabolism: Ojibwa, 14.6 mug/ml; Chinese, 10.0 mug/ml; and Caucasians, 9.4 mug/ml. The high rate of ethanol metabolism in Amerind subjects differs from previous findings. Habitual level of alcohol consumption, proportion of body fat and genetic factors appear to account for most of the group differences.

Acetaldehyde↗
PubMed1975

A possible major contribution to mental retardation in the general population by the gene for microcephaly.

In a study of 13 families with genetic microcephaly, it was found that 11 of 24 parents (two fathers not ascertained) and 11 of 33 non-microcephalic siblings were of subnormal intelligence. In a rare autosomal recessive condition, all parents and two-thirds of unaffected siblings are presumed carriers of the gene. It so, nearly 50% of all presumed heterozygotes in the present study were mentally retarded. The proportion agrees well with the other major study of microcephaly in North America, but differs from the Dutch study. On the basis of pooled data from the three studies and the estimated incidence of 1:40000 for genetic microcephaly, it is postulated that (1) about 0.34% of the general population is mentally retarded because it is carrying the gene for microcephaly and (2) about one of nine mentally retarded individuals is heterozygous for the gene for microcephaly.

Adolescent↗