Autor: |
Adebayo GI; Department of Therapeutics, Trinity Centre for Health Sciences, St. James's Hospital, Dublin, Ireland., Gaffney P, Feely J |
Jazyk: |
angličtina |
Zdroj: |
Alcohol (Fayetteville, N.Y.) [Alcohol] 1996 Nov-Dec; Vol. 13 (6), pp. 597-602. |
DOI: |
10.1016/s0741-8329(96)00074-2 |
Abstrakt: |
The effect of a single dose of alcohol (0.8 g/kg), given with "diet coke," on erythrocyte sodium-lithium countertransport (SLC) in relation to membrane cholesterol and phospholipids was assessed over 24 h in 10 healthy volunteers. Baseline passive lithium efflux (0.168 +/- 0.008 mmol l-1 Cell H-1) was increased 1 h (0.202 +/- 0.014 mmol l-1 cell h-1; p < 0.030), and 4 h (0.200 +/- 0.014 mmol l-1 cell h-1; p < 0.020), but similar to that at 24 h postalcohol (0.173 +/- 0.011 mmol l-1 cell h-1). These changes were not associated with any change in intracellular lithium. Control SLC VMAX of 0.387 +/- 0.054 mmol l-1 cell h-1 fell at 1 h (0.328 +/- 0.050 mmol l-1 cell h-1; p = 0.0012) and 4 h (0.312 +/- 0.048 mmol l-1 cell h-1; p < 0.0005). Its value 24 h postalcohol (0.371 +/- 0.047 mmol l-1 cell h-1) was comparable to that at baseline. There was no significant change in the affinity of the transporter for external sodium throughout the experimental period, suggesting that the reduction in VMAX 1 and 4 h after alcohol ingestion resulted from a noncompetitive inhibition. Intracellular sodium 4 h after alcohol was lower than at baseline, but returned to the control value within 24 h. In a control group (n = 5), pretreatment with "diet coke" alone did not alter any of the measured parameters. It is concluded that alcohol pretreatment increases passive lithium efflux and decreases SLC Vmax. Both effects are evident up to at least 4 h postdosing, but recover within 24 h in the absence of further alcohol intake. |
Databáze: |
MEDLINE |
Externí odkaz: |
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