Regulation of intracellular magnesium by Mg2+ efflux.

Zusammenfassung: Bei chronischem Mg-Mangel sinkt im Herzmuskel der Gehalt an Mg) und K Der Gehalt an Ca, Na und Hydroxyprolin nimmt zu Im Harn werden Adrenalin und besonders Noradrenalin vermehrt ausgeschieden Gleichzeitiger Larmstres verstarkt diese Veranderungen Die Effekte nehmen mit dem Grade des Mg-Mangels zu Die Anderungen des Na-, K*-, Ca-, Mgund Hydroxyprolin-Gehaltes korrelieren mit der Ausscheidung von Noradrenalin Die Vermehrung des Kollagengehaltes lies sich elektronenmikroskopisch verifizieren und auf eine Stimulierung von Fibrocyten zuruckfuhren

/pdf/elektrolyt-und-kollagengehalt-im-rattenherzen-bei-3b0o00x8c7.pdf

Elektrolyt- und Kollagengehalt im Rattenherzen bei chronischem Magnesium-Mangel und Streß

The natural course of hypertrophic cardiomyopathy is usually characterized by variable degrees of progression [10, 11, 18]. Long-term therapy with beta-blocking agents has proved to be disappointing [3, 11]. Surgical intervention led to initial improvement in many patients, but complaints may reappear with time [17]. These therapeutic strategies thus seem unable to influence either the progression or the long-term prognosis of the disease.

Verapamil Treatment of Hypertrophic Cardiomyopathy

Increase of collagen in the rat heart induced by noise

It is a well-known fact that hypertrophy of both ventricles as well as disseminated or confluent myocardial necroses can be experimentally produced in rats by overdoses of the β-adrenergic stimulant isoproterenol. Thus not only cardiomyopathic Syrian hamsters [1,2], but also isoproterenol-treated hypertrophic rat hearts are valuable disease models for pathophysiological studies on hypertrophic cardiomyopathy.

Prevention by Verapamil of Isoproterenol-Induced Hypertrophic Cardiomyopathy in Rats

1. 2,4,7-Triamino-6-phenyl-pteridine (triamterene) protects the rat heart against isoproterenol-induced myocardial lesions: Whilst cardiotoxic doses of isoproterenol produce deleterious myocardial Ca overload, simultaneous admistration of triamterene diminishes myocardial Ca incorporation considerably. 2. As to the mechanism of action, triamterene increases the plasma contents of K and Mg by inhibiting renal excretion. Accordingly, oral administration of K and Mg salts, leading to a similar rise in the K and Mg concentrations of the plasma, also prevents abundant myocardial Ca incorporation. 3. Cardioprotection by triamterene can, in fact, be simply explained by its action on the plasma K and (particularly) Mg levels. This conclusion is drawn from a quantitative comparison of the inhibitory effects of triamterene (40 mg/kg s.c.) with those of KCl or MgCl2 (10 mMol/kg p.o.) on the isoproterenol-induced increase in myocardial 45Ca uptake and absolute Ca concentration. 4. Isoproterenol induced cardiomyopathy of the rat, an experimental model of non-coronarogenic myocardial lesions, has hitherto been successfully prevented with the use of Ca-antagonists (verapamil, D 600, prenylamine, fendiline). These compounds reduce Ca influx by restricting the Ca conductivity of the myocardial sarcolemma membrane ("slow channel"). The action of triamterene, on the other hand, is based on a totally different cardioprotective principle, namely competitive inhibition of intracellular myocardial Ca accumulation via an increase in K and Mg supply. In the future treatment of cardiomyopathy it seems rather promising to try a combination of both a Ca-antagonist and triamterene, thus applying two different therapeutic principles simultaneously.

[Mechanism of the cardioprotective effect of triamterene in the rat heart. Myocardial protection via elevation of extracellular K+ and Mg++ concentrations].

Die durch chron. Isoproterenol-Gaben (7 Tage tagl. 1 mg/kg s.c.) erzeugte Cardiomegalie geht mit einer Hypertrophie beider Ventrikel einher. Im rechten Ventrikel stieg der Herzindex (Ventrikelgew. (mg) Korpergew. (g)) von 0,56 auf 0,8 an; links erhohte sich der Herzindex von 2,02 auf 2,65 (n = 157). Auserdem kommt es in der Herzspitze zur Ausbildung vernarbender subendothelialer Nekroseherde, die durch Anstieg der Hydroxyprolin-Krozentration quantitativ erfast wurden. Gleichzeitige Gaben von Verapamil (15 mg/kg s.c.) konnen die hypertrophische Cardiomyopathie witgehend verhuten. Peroral verabreichte K+- und Mg++-Salze (2 x tagl. 12,5 mMol/kg) uben als naturliche Ca++-Antagonisten analoge Schuzeffekte aus. Eine optimale Cardioprotektion ist in der Kombination von KCI bzw. MgCl2 mit Verapamil erreichbar.

Schutzeffekt von Ca++-Antagonisten bei der Isoproterenol-induzierten hypertrophischen Cardiomyopathie der Ratte

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[Mechanism of the cardioprotective effect of triamterene in the rat heart. Myocardial protection via elevation of extracellular K+ and Mg++ concentrations].

Schutzeffekt von Ca++-Antagonisten bei der Isoproterenol-induzierten hypertrophischen Cardiomyopathie der Ratte