Sila-Procyclidin (1 b) sowie dessen Derivate 2 b (Sila-Trihexyphenidyl), 3 b und 4 b (Sila-Cycrimin) wurdenausgehend von C13SiCH2CIdurch eine neue, sechsstufige Synthese mit einer Gcsamtausbeute von 16 (lb). 19 (Zb), 8 (3b) bzw. 7% (4b) dargcstellt. -Verglcichende in-vivo-Untenuchungen (Maus, per-os-Applikation) hinsichtlich der peripheren und zentralen anticholinergen Wirkung haben gezcigt. daO die Silicium-Verbindung 1 b dem Kohlenstofl-Analogon 1 a (Procyclidin) iiberlegen ist.
In the rat, the antiulcer potencies of the M1antimuscarinics telenzepine and pirenzepine, the H2 receptor blocker cimetidine, and the H+/K+-ATPase inhibitor omeprazole were compared with their antisecretory potencies. On a molar basis and with regard to inhibition of cysteamine-induced acid secretion, telenzepine ranked first, followed by omeprazole, cimetidine, and pirenzepine; cysteamine-induced duodenal ulcers were best inhibited by telenzepine, with pirenzepine, omeprazole and cimetidine ranking 2nd, 3rd and 4th. Up to the highest dose tested, cimetidine and omeprazole caused inhibition by 26 and 37%, respectively. While, with the antimuscarinics, lesion inhibition runs parallel with inhibition of acid secretion, the H2 receptor blocker and the H+/K+-ATPase inhibitor markedly impair acid secretion, but do not or merely negligibly inhibit cysteamine-induced formation of duodenal ulcers. This suggests that in this animal model the antiulcer effect cannot be attributed exclusively to the antisecretory action.
A direct comparison of the ulcer-healing effects of two H+-K+-ATPase inhibitors (pantoprazole and omeprazole), one M1 antimuscarinic (telenzepine) and one H2 receptor antagonist (cimetidine) was performed in the rat. Gastric and duodenal ulcers were induced by local application of acetic acid and thereafter treated over 10 days by the test drugs. Overall and on a molar basis, ulcer healing was comparably accelerated by pantoprazole, omeprazole and telenzepine and less so by cimetidine. The same rank order was found with respect to the inhibition of gastric acid secretion in the modified Shay rat.
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