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Biomedical subjects

W Landauer

Publications and source records attributed to W Landauer.

18 recordsLinked to original sources
PubMed1978

Cholinomimetic teratogens. VI. The interaction of cholinomimetic teratogens with the antimalarial drugs chloroquine and chlorguanide.

A typical syndrome of short and crooked neck together with muscular hytoplasia of the legs occurs with low incidence in chicken embryos following injection into the egg at 24 hours of incubation of the antimalarial drug chloroquine; but treatment at later stages does not have similar effects. When, however chloroquine was used in addition to carbachol or neostigmine at 96 hours of incubation the malformations caused by the two cholinomimetic compounds, i.e., carbachol and neostigmine, occurred with greatly increased frequency and tended also to be exaggerated in expression. Chlorguanide, another antimalarial drug, when used as additive, reduced the teratogenic effects of such compounds as decamethonium and neostigmine. It appears that the neuromuscular pathways to teratogenicity are for carbachol and neostigmine and for chloroquine clearly related, if at different levels of expressivity.

Abnormalities, Drug-Induced↗
PubMed1977

Cholinomimetic teratogens. V. The effect of oximes and related cholinesterase reactivators.

Pyridine-2-aldoxime methiodide and pyridine-2-aldoxime methyl methane sulfonate (P2S) used as supplements to carbachol or neostigmine, greatly lowered the incidence of chicken embryos of vertebral defects and muscular hypoplasia. With 4-pyridine aldoxime the effect of the teratogens was less reduced. Supplementation of carbachol or neostigmine with either ambenonium or toxogonin lessened the occurrence of muscular hypoplasia, but did little, if anything, to prevent malformation of the neck vertebrae. In tests with physostigmine P2S as supplement reduced or prevented cervical defects, but failed to protect the nicotinamide-sensitive parts of the embryo.

Abnormalities, Drug-Induced↗
PubMed1976

Cholinomimetic teratogens. III. Interaction with amino acids known as neurotransmitters.

The amino acids gamma-aminobutyric acid, taurocholate, guanidine, glycine, and beta-alanine, known to have putative functions as neurotransmitters, when given as supplement to carbachol or decamethonium, greatly reduced the incidence of malformations produced in chicken embryos by these depolarizing cholinomimetic teratogens. In combination with the nondepolarizing teratogens neostigmine and pyridostigmine similarly beneficial effects occurred only by supplementation with gamma-aminobutyric acid.

Alanine↗
PubMed1976

Cholinomimetic teratogens. IV. Effects of the genotype for muscular dystrophy in chickens.

Embryos of a family of chickens homozygous for muscular dystrophy (md/md) reacted with a higher incidence of malformations to treatment with carbachol than did White Leghorn embryos. The same difference in response of embryos from the two stocks occurred after treatment with sulfanilamide. Embryos of reciprocal crosses between these two stocks differed greatly, however, in their response to carbachol, F1 embryos from dystrophic hens producing a much higher incidence of malformations than did those from Leghorn hens. In contrast, both F1 sibs reacted similarly to sulfanilamide, the teratogenic effects being intermediate between those of embryos from the parent stocks.

Abnormalities, Drug-Induced↗
PubMed1975

Cholinomimetic teratogens: studies with chicken embryos.

The cholinomimetic compounds carbachol, decamethonium, neostigmine, succinylcholine, trimethylphenylammonium, and others were tested for their interference with normal chick development. All these compounds led to abnormalities of the cervical vertebrae; at higher dosage interference with normal morphogenesis involved the whole vertebral column. Hypoplasia of the leg muscles occurred with lower incidence. Responses, tested with carbachol, rose from 24 to 72 and 96 h, then declined to 120 h of incubation. Two of the cholinometic compounds used in combined treatment produced a high degree of synergism. Gallamine, benzoquinomium, butyrylcholine, and bethanechol had protective effects. Acetylcholine, at high dosage, caused defects different from the above. It is suggested that the cholinomimetic teratogens interfere with normal development by displacing acetylcholine from its receptors or by forming complexes with it.

Acetylcholine↗
PubMed1975

Cholinomimetic teratogens. II. Interaction with inorganic ions.

Treatment of chicken embryos after 96 h of incubation showed that the teratogenic activity of the cholinomimetic compounds carbachol, neostigmine, decamethonium, and tetramethylammonium is reduced in the presence of calcium acetate. Similarly, supplementation with potassium acetate reduced the teratogenicity of carbachol and tetramethylammonium.

Abnormalities, Drug-Induced↗