US EPA

2951690 

Journal Article 

A central vasodepresser effect of Dyflos 

Edery, H; Guertzenstein, PG 

1974 

Yes 

British Journal of Pharmacology
ISSN: 0007-1188
EISSN: 1476-5381 

50 

4 

481-487 

English 

4614881 

The vasodepressor effects of dyflos (55914) were studied in cats. Male cats were anesthetized and atropinized peripherally by the intravenous injection of 2 milligrams per kilogram atropine-methyl-nitrate (52880). Dyflos was applied by means of perspex rings topically placed on the ventral surface of the brain for doses of 1 to 20 milligrams per milliliter (mg/ml). Blood pressure and heart rate were determined. The effects of atropine-methyl-nitrate, also applied in perspex rings, on the depression caused by dyflos were studied using 50mg/ml. Reactivators of acetylcholinesterase obidoxime (7683365), pralidoxime-mesylate, and another pyridinium/aldoxime, compound-30, were applied topically in the same way at 100 to 200mg/ml to study the moderations of the depressor effect. Obidoxime and pralidoxime-mesylate were also used against the vasodepression caused by carbachol (51832) or glycine (56406) applied to the ventral surface of the brain. The topical application of dyflos at any dose caused a fall in arterial blood pressure without any change in heart rate. The vasodepressor effect was prevented by the topical application of atropine-methyl-nitrate. Applied in the same way, obidoxime and pralidoxime-mesylate, but not compound-30, abolished the vasodepressor effect of dyflos. Obidoxime and pralidoxime-mesylate also reversed the vasodepression caused by carbachol but not that of glycine. The authors conclude that the fall in blood pressure caused by dyflos is due to a decrease in sympathetic vasomotor tone whether caused by acetylcholinesterase reactivation or a central atropine like reaction.