Alcohol and Alcoholism Advance Access published online on October 31, 2005
Alcohol and Alcoholism, doi:10.1093/alcalc/agh228
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 BioMag Laboratory, Helsinki University Central Hospital; Cognitive Brain Research Unit, University of Helsinki, Finland
* To whom correspondence should be addressed. Aim: To present findings on the kinetics and dynamics of cardiovascular drugs during alcohol withdrawal (AW), compared with that observed in remission. Method: Studies were reviewed and summarized. Results: A single-dose study in alcoholic patients with propranolol, a
Received May 11, 2005
Revised August 23, 2005
Accepted October 7, 2005
Commentary
RESPONSES TO CARDIOVASCULAR DRUGS DURING ALCOHOL WITHDRAWAL
SEPPO KÄHKÖNEN, E-mail: seppo.kahkonen{at}helsinki.fi
![]()
Abstract
-adrenergic antagonist, showed that the negative inotropic effect was decreased and the bradycardiac effect increased during AW as compared with during early remission. The hypotensive effect of isosorbid dinitrate, commonly used as a vasodilatator, was weaker at the onset of AW, being associated with the decreased bioavailability of the drug. Verapamil, which is a L-type Ca2+ channel antagonist, produced a bradycardiac effect at the onset of AW, but no effect was observed in early remission. The effect was probably due to changes in L-type Ca2+ channels because no differences in verapamil concentrations between AW and early remission were observed. Conclusion: Taken together, AW modifies the dynamics and kinetics of cardiac drugs, which may have an impact on the treatment of alcoholic patients with cardiac diseases.![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
A McKeon, M A Frye, and N. Delanty The alcohol withdrawal syndrome J. Neurol. Neurosurg. Psychiatry, August 1, 2008; 79(8): 854 - 862. [Abstract] [Full Text] [PDF] |
||||
