The intraperitoneal administration of d-propoxyphene HCI to albino mice at a dosage level of 200 mg./Kg. was lethal to all 80 controls. The prophylactic subcutaneous administration of either nalorphine HCI, levallorphan tartrate, or methylene blue produced a significant increase in the number of survivors and also increased significantly the mean survival time of the remainder. Methylene blue in combination with nalorphine HCI potentiated the protective effect of nalor hine HCI, while the dye in combination with levallorphan tartrate reduced the antigtal effectiveness of the latter. Neither malachite green oxalate nor quinacrine dihydrochloride was able to produce significant protection against lethal doses of d-propoxyphene.
HE PHARMACOLOGICAL properties of a-dl-4-"dime thy lamino -1,2diphenyl -3methyl-2-propionyloxybutane (dl-propoxyphene) were fist described in 1955 by Robbins, who reported that oral and subcutaneous doses of this compound produced a profound morphine-type analgesia in rats and dogs without the development of tolerance (1). After resolution of the optically active isomers, the dextro isomer (dpropoxyphene) exhibited twice the analgesic potency of the isomeric mixture on a weight basis, while the lev0 isomer was ineffective ( 2 ) .
Clinically, d-propoxyphene was shown to produce effective analgesia similar to that of codeine when administered orally as the hydrochloride salt alone or in combination with acetophenetidin, acetylsalicylic acid, and caffeine In March 1960, the National Clearinghouse for Poison Control Centers reported a total of 12 cases of accidental ingestion and acute overdosage of d-propoxyphene (6). Since that time, a number of additional episodes have appeared in the literature (7-9). Even with quantities many times greater than the therapeutic dose, relatively rapid recoveries were made if gastric lavage and symptomatic therapy were instituted before the onset of coma or convulsions. A more serious clinical picture occurred with the ingestion of extremely large amounts or a delay in the initiation of symptomatic therapy.
There is no specific antidote for d-propoxyphene
(3-5).