Pharmakodynamische Grundlagen der Therapie mit herzwirksamen Glykosiden

Rothlin, E.; Bircher, R.

doi:10.1007/978-3-642-94621-9_7

Cited by 28 publications

(7 citation statements)

References 146 publications

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“…The pathological alterations of brain tissue caused by ouabain are comparable to those described in cardiac muscle. Rothlin and Bircher (1954) found degenerative alterations in the heart with signs of inflammatory infiltration. Particularly the cells of the conductile tissue of the heart were vacuolized and their plasma was homogenized, even when glycosides were administered chronically and even before any ECG alteration.…”

Section: ( 1 ) Histopathological Aspectsmentioning

confidence: 97%

The Epileptogenic Effect of Ouabain (g‐Strophanthin) Its Action on the EEG and Cortical Morphology

Petsche¹,

Rappelsberger²,

Frey³

et al. 1973

Epilepsia

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SUMMARY Local application of ouabain in agar on the cerebral cortex elicits generalized seizures. Progressive deterioration of the uppermost cortical layers takes place, related in extent and degree to the concentration of the drug and duration of application. The seizure patterns under ouabain start earlier and are more apt to be of hippo‐campal type when the concentration of the drug is high. The decrease in voltage of the seizure activity is related to the increasing number of neurons destroyed. Finally relations between EEG and clinical seizure patterns are described. Particularly in later stages of status epilepticus, the relation between cortical transients and jerks of the limbs decreases, and the conclusion is drawn that deep brain centers increasingly take over the role of pace‐makers for myoclonic jerks. The results are discussed with respect to the mechanisms both of the action of ouabain and of neurophysiological events during ouabain seizures. RÉSUMÉ Ľapplication locale ďouabaine sur agar, sur le cortex cérébral provoque des crises généralisées. Une détérioration progressive des couches corticales les plus super‐ficielles prend place, liééàľétendue et au degré de concentration de la drogue et à la durée de ľapplication. Les types de crises sous ouabaíne apparaissent plus précocement et sont plutôt de type hippocampien, ďautant plus que la concentration de la drogue est plus élevée. La diminution de voltage de ľactivité critique est en relation avec ľaugmentation du nombre de neurones détruits. Ensuite les relations entre les patterns EEG et les crises cliniques sont décrites. En particulier dans la période tardive des états de mal, on observe une diminution des relations entre les décharges corticales et les secousses des membres. On tire la conclusion que les structures cérébrales profondes prennent progressivement le rôle de plus en plus important, comme pace‐maker dans ľorigine des secousses myocloniques. Les résultats sont discutés en ce qui concerne les mécanismes à la fois de Taction de ľouabaïne et des phénomènes neurophysiologiques pendant les crises provoquées par ouabaïne. ZUSAMMENFASSUNG Lokale Applikation von Ouabain in Agar auf den Cortex verursacht generalisierte Anfälle. Es kommt zu einer zunehmenden Zerstörung der oberflächlichen kortikalen Schichten, deren Ausmass von der Konzentration des Ouabains und der Dauer der Einwirkung abhängt. Die Anfallsmuster beginnen umso früher, je stärker die Konzentration von Ouabain ist. Die Amplitudenabnahme, die im Lauf des Status eintritt, steht in Beziehung zur Anzahl der Neuronen, die durch Ouabain zerstört werden. Die Beziehungen zwischen EEG‐Mustern und klinischem Anfallsmuster werden untersucht. Besonders in Spätstadien des Status epilepticus nimmt die anfangs so klare Beziehung zwischen korticalen Entladungen und Myoklonismen ab, woraus gefolgërt wird, dass nun Regionen in der Tiefe des Gehirns mehr und mehr die Rolle von Pace‐makers für die Myoklonismen iibernehmen. Die Ergebnisse werden diskutiert im Hinblick auf die Mechanismen der Ouabain...

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Section: ( 1 ) Histopathological Aspectsmentioning

confidence: 97%

The Epileptogenic Effect of Ouabain (g‐Strophanthin) Its Action on the EEG and Cortical Morphology

Petsche¹,

Rappelsberger²,

Frey³

et al. 1973

Epilepsia

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“…Digoxin was chosen because it has intermediate properties and is the glycoside most widely, prescribed in this country. A single experiment on lanatoside C was included because it has been claimed to have exceptionally low toxicity (Fahr & La Due, 1941;Rothlin & Bircher, 1954). Calactin, which is not used therapeutically, was included in the study because of its apparent biological role as an emetic toxin.…”

Section: Discussionmentioning

confidence: 99%

Cat assay for the emetic action of digitalis and related glycosides (digitoxin, digoxin, lanatoside C, ouabain and calactin)

Parsons

Summers

1971

British J Pharmacology

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Summary1. A titration assay with two end points is described for comparison of the emetic and lethal potencies of digitalis-like drugs. 2. A drug was infused at constant rate to a conscious, unrestrained cat. through an indwelling venous cannula. At the moment of vomiting the cat was rapidly anaesthetized and infusion continued at the same rate until the moment of cardiac arrest. 3. With very slow and very fast infusions, the emetic and lethal doses tended to rise. In the range between these extremes (which varied from drug to drug) they were independent of time. 4. The observations could be accounted for by analogue computation, assuming that the drugs entered an initial pool and were distributed at finite rates to receptors in the CNS (vomiting centre) and heart. 5. Half times of metabolic loss derived from this computation for digitoxin, digoxin and ouabain (17, 9 9 and 1-8 h, respectively) were in the same ratio as the threefold longer half times reported for these drugs in man. 6. When measured with infusion rates in the time independent range, the ratio of lethal to emetic doses did not vary between the drugs studied. All caused vomiting at 40% of the lethal dose. 7. From a review of the literature, the emetic and cardiotoxic actions of digitalis-like drugs appear inseparable and probably share a common biochemical mechanism. 8. It is concluded that foreseeable improvements in digitalis-like drugs are small and would depend on the elimination of any local emetic effect on gut receptors which they may have.

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“…Previous experimental phar macodynamic studies of a-AD deal with the acute toxicity [31], the enteral resorption (cats) [14], the effects on cardiac rhythm [31] and the distribution and excretion in rats [4,5] and in dogs [21]. However, no experimental data are available on the effects of a-AD on cardiovascular dynamics and on heart metabolism in intact animals.…”

mentioning

confidence: 99%

“…Blood glucose was determined enzymatically according to Slcin [31] and the plasma FFA titrated as reported by Dole and Meinerts [10], Blood samples (arterial and coronary venous blood) were taken before and at 10-minute intervals following the i.v. administration of 0.05 and 0.1 mg/kg a-AD respectively.…”

mentioning

confidence: 99%

The Effects of α-Acetyldigoxin on Cardiac Dynamics and Myocardial Glucose and Free Fatty Acid Extraction in Nonfailing Dogs

Kraupp¹,

Raberger²,

Chirikdjian³

1968

Pharmacology

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Pharmakodynamische Grundlagen der Therapie mit herzwirksamen Glykosiden

Cited by 28 publications

References 146 publications

The Epileptogenic Effect of Ouabain (g‐Strophanthin) Its Action on the EEG and Cortical Morphology

The Epileptogenic Effect of Ouabain (g‐Strophanthin) Its Action on the EEG and Cortical Morphology

Cat assay for the emetic action of digitalis and related glycosides (digitoxin, digoxin, lanatoside C, ouabain and calactin)

The Effects of α-Acetyldigoxin on Cardiac Dynamics and Myocardial Glucose and Free Fatty Acid Extraction in Nonfailing Dogs

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