Abstract:
:Low concentrations of ethanol (17 mM) inhibited development of spontaneous mechanical activity (vasomotion) in isolated rat portal veins. Low concentrations of ethanol potentiated, however, contractions induced by epinephrine, but not those induced by angiotensin or potassium. Higher concentrations of ethanol, such as those associated with surgical anesthesia (100-170 mM), resulted in almost complete suppression of spontaneous contratile responses. These higher concentrations of ethanol: a) attenuate contractions induced by epinephrine, angiotensin, and potassium (K+); b) cause noncompetitive displacement of the dose-response curves of these vasoactive compounds; c) attenuate calcium (Ca++)-induced contractions of K+-depolarized portal veins; d) relax drug-induced, as well as Ca++-induced, contractions of portal veins. The profound depressant actions of ethanol are not mimicked by alpha-adrenergic, histaminergic, cholinergic, or serotonergic blocking drugs, nor are they attributable to actions on beta-adrenergic receptors. The direct vasodepressant actions of ethanol on isolated venous smooth muscle may play a significant role in alcohol-induced peripheral vasodiatation seen in man and animals.
journal_name
Anesthesiologyjournal_title
Anesthesiologyauthors
Edgarian H,Altura BMdoi
10.1097/00000542-197604000-00009subject
Has Abstractpub_date
1976-04-01 00:00:00pages
311-7issue
4eissn
0003-3022issn
1528-1175journal_volume
44pub_type
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