EinleitungStörungen der Aufmerksamkeit, der Merkfähigkeit, des Reaktionsvermögens und des problemlösenden Denkens spielen für die Behandlung, Prognose und Rehabilitation schizophrener Erkrankungen schon seit langem eine herausragende Rolle [1]. Ent-sprechende kognitive Defizite bei affektiven Erkrankungen sind erst in den letzten Jahren in den Blickpunkt des Interesses geraten [2 ± 4]. Bei der Suche nach den Ursachen dieser teils reversiblen, teils irreversiblen kognitiven Symptome fällt das Augenmerk u. a. auch stets auf den Faktor Medikation. Die Frage nach Art und Ausmaû möglicher pharmakologischer Einflüsse auf
Afferent nerve fibre activity from left ventricular mechanoreceptors was recorded in 10 anaesthetized cats before and after two intravenous injections of 15 micrograms/kg digoxin at 1 hour interval. These receptors are activated by coronary artery occlusion and induce a depressor cardiovascular reflex resulting in bradycardia and hypotension. Neither the spontaneous activity of the receptor's afferent nerve fibres nor their maximum activity during temporary coronary artery occlusion was affected by digoxin. The results show that digoxin in therapeutic doses has no sensitizing effect on left ventricular mechanoreceptors with vagal afferent fibres. The sensitization of cardiopulmonary baroreflexes by digitalis glycosides shown in previous investigations is thus more likely to be mediated by a central nervous effect of the drug.
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