Biomedical subjects

H Wick

Publications and source records attributed to H Wick.

At least 55 records · Page 3Linked to original sources

PubMed1976

[General pharmacology and secretion inhibitory action of (8r)-3alpha-hydroxy-8-isopropyl-1alphaH,5alphaH-tropanium bromide-(+/-)-tropate (ipratropiumbromide) (author's transl)].

(8r)-3alpha-Hydroxy-8-isopropyl-1alphaH,5alphaH-tropaniumbromide-(+/-)-tropate (ipratropiumbromide, Sch 1000) is a quaternary tropic acid tropane ester with pronounced anticholinergic activities (inhibition of secretion and spasmolysis). The effect of the substance of all parasympathetically innervated organs ist 1.4 to 2 times stronger than that of atropine. As an inhibitor of the secretion of free hydrochloric acid in the stomach it proved to be 5 times more effective than atropine. Central activities were not observed. The duration of action of Sch 1000 exceeds that of atropine by far.

Animals↗

PubMed1976

[The effect of (8r)-3alpha-hydroxy-8-isopropyl-1alphaH,5alphaH-tropaniumbromide-(+/-)-tropate ((ipratropiumbromide) on tracheobronchial spasm, bronchial and salivary secretions, ECG and heart rate (author's transl)].

At very low doses (8r)-3alpha-hydroxy-8-isopropyl-1alphaH,5alphaH-tropaniumbromide-(+/-)-tropate (ipratropiumbromide, Sch 1000, Atrovent) and atropine inhibit acetylcholine-induced bronchospasms in guinea-pigs and dogs. The dose ratio main effect vs. most sensitive side effect (inhibition of saliva secretion) is 1:10 for i.v. injection and 1:100 for aerosol application. When both compounds are administered in a nebulized form bronchodilatation occurs immediately. The maximum effect of Sch 1000 occurs somewhat later than that of atropine but the duration of action is much longer. Bronchial secretion in guinea-pigs is increased by small doses of Sch 1000 and atropine. These doses correspond to bronchodilating doses.

Acetylcholine↗

PubMed1975

Stereoisomeric 5,9-dimethyl-2'-hydroxy-2-tetrahydrofurfuryl-6,7-benzomorphans, strong analgesics with non-morphine-like action profiles.

The eight optically active stereoisomers and the corresponding four racemic forms of 5,9-dimethyl-2'-hydroxy-2-tetrahydrofurfuryl-6,7-benzomorphan (1) have been prepared. Depending on their configurations these compounds are potent analgesics or inactive substances in mice. The analgesics attain potencies up to about a hundred times that of morphine but they do not show morphine-like side effects in mice nor do they suppress abstinence in withdrawn morphine dependent monkeys. Their therapeutic ratios are favorable and, in the case of la-1 and la-2, exceptionally good. Configuration-activity relationships are discussed. R configuration of the N-tetrahydrofurfuryl group is a major prerequisite for high analgesic potency.

Analgesia↗

PubMed1975

Acute neonatal nonketotic hyperglycinemia: normal propionate and methylmalonate metabolism.

Propionyl-CoA carboxylase and combined methylmalonyl-CoA (MMA-CoA) racemase and -mutase activities were studied in liver and fibroblasts of two patients with the acute neonatal form of nonketotic hyperglycemia. In all experiments, these enzyme activities studied in tissues of the patients were within the range of healthy control subjects, whereas no propionyl-CoA carboxylase activity was measurable in the fibroblasts of a patient with propionic acidemia. Subcellular fractionation of liver and fibroblasts indicated that the normal amounts of MMA-CoA found after incubation of whole tissue homogenate were formed by propionyl-CoA carboxylase, a mitochondrial enzyme, and not be acetyl-CoA carboxylase, which theoretically could also be involved in the carboxylation of propionyl-CoA. From the above data as well as from clinical and biochemical observations in three patients, it was concluded that there exists a true nonketotic hyperglycinemia which is not related etiologically to the different disorders of the ketotic hyperglycinemia syndrome. True nonketotic hyperglycinemia is not associated with ketoacidosis even after loading with propionate- and MMA precursors. It must be distinguished by exclusion from mild forms of the ketotic hyperglycinemia syndrome which may present clinically as hyperglycinemia without ketosis.

Acute Disease↗

PubMed1974