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Alcohol and Alcoholism Vol. 36, No. 5, pp. 377-380, 2001
© 2001 Medical Council on Alcohol

CHOLINERGIC NERVES MEDIATE ACETALDEHYDE ACTION IN THE GASTROINTESTINAL TRACT

Hiroshi Kinoshita,*, Iwao Ijiri1, Setsuko Ameno1, Takako Kubota1, Xia Zhang1, Shigeru Hishida and Kiyoshi Ameno1

Department of Legal Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo, 663-8501 and
1 Department of Forensic Medicine, Kagawa Medical University, 1750-1, Miki, Kita, Kagawa, 761-0793, Japan

Received 15 March 2000; first review notified 5 March 2001; accepted 31 March 2001

— The regulation mechanism of inhibition of intestinal ethanol absorption induced by high acetaldehyde (AcH) concentration in blood was investigated. We used atropine (AT), atropine methylbromide (ATMB), pirenzepine (PI), bethanechol (BE) and pilocarpine (PL) with or without cyanamide (CY; a potent inhibitor of aldehyde dehydrogenase, which induces high AcH concentration in blood). The Ka (absorption rate constant) value after the CY-alone pretreatment was significantly lower than that in controls. In the high AcH-induced cases, the values of Ka in AT and ATMB pretreatments were similar to controls, but the value of Ka in PI pretreatment was lower than that in controls. The values of Ka in the case of BE pretreatment with and without high AcH levels were lower than in controls. The Ka value in the PL with CY was significantly lower than that with CY alone. However, its action was blocked by ATMB pretreatment. These results suggest that high blood AcH concentrations inhibit intestinal ethanol absorption through the peripheral cholinergic nerves via muscarinic receptors, except for the muscarinic M1 receptor, compared to other subtypes of muscarinic receptors.


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