Calcium accumulates in muscles of dystrophic hamsters (DH) and patients with Duchenne muscular dystrophy. Various Ca antagonists were beneficial to the cardiomyopathy of DH, but had only minor effects on skeletal muscle. We administered a new Ca antagonist, diltiazem, 25 mg/kg/day orally to normal and dystrophic hamsters from ages 37 to 92 days. We observed a marked reduction in muscle Ca in DH treated with diltiazem: 73% in the heart, 61% in the diaphragm, and 48% in the rectus femoris. Plasma CK was significantly lower (by 37%) in treated DH, while the elevated rate of noncollagen protein synthesis in the diaphragm was not diminished. Histologically, the most important change was a reduction in Ca deposits in the heart. Diltiazem was well-tolerated by all animals and did not modify Ca content in normal hamsters. This study suggests that diltiazem may have therapeutic value in those conditions that are accompanied by excessive accumulation of Ca in tissues, such as muscular dystrophy.

The effects of diltiazem in dystrophic hamsters.

Influence of the pH of cardioplegic solutions on intracellular pH, high-energy phosphates, and postarrest performance. Protective effects of acidotic, glutamate-containing cardioplegic perfusates.

Evidence of a new, preferentially Mg-carrying, transport system besides the fast Na and the slow Ca channels in the excited myocardial sarcolemma membrane

Pro: magnesium is a valuable therapy in the cardiac surgical patient.

The pathophysiology of congestive heart failure (CHF) includes conditions (e.g., activation of the renin-angiotensin-aldosterone system) which, when combined with CHF therapies, make patients afflicted with this syndrome quite susceptible to electrolyte disturbances. The most commonly encountered are hyponatremia, hypokalemia, and hypomagnesemia. These derangements are of vast clinical importance; their development not only represents an immediate threat to the CHF patient (e.g., dysrhythmias secondary to hypokalemia), but are also indicative of underlying pathophysiologic events, an unfavorable clinical course, and occasionally an adverse therapeutic response. The optimal care of CHF patient includes the recognition and management of these electrolyte disturbances.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/clc.4960180704

Electrolyte disturbances in chronic heart failure: metabolic and clinical aspects

The crucial point in the pathogenesis of isoproterenol-induced myocardial necrotization is an abundant intracellular Ca accumulation leading to high energy phosphate exhaustion. Accordingly, in the early stage of the isoproterenol-induced necrotization process, the onset of ATP and creatine phosphate breakdown strictly parallels the acute Ca gain. In this type of necrosis, the Mg losses from the myocardium appear as a concomitant phenomenon. The hearts can be protected against the deleterious Ca overload and necrotization by increasing the plasma concentration of Mg, K, or H ions in order to counterbalance Ca according to the ration (see article). On the other hand, if Mg, K, or H ion concentrations are too low, isoproterenol-induced Ca uptake and myocardial lesions are potentiated.

Prevention of myocardial Ca overload and necrotization by Mg and K salts or acidosis.

As shown in previous investigations overdoses of isoproterenol produce an abundant myocardial Ca uptake, followed by high energy phosphate breakdown, mitochondrial damage and, eventually, cardiac fibre necrotization. Conversely Ca antagonistic compounds such as verapamil, D 600 or prenylamine which reduce the transmembrane Ca influx into the heart muscle cells, can prevent high energy phosphate deficiency and cardiac lesions. Ethyl-4-(3,4,5-trimethoxycinnamoyl) poperazinyl acetate (Vascoril) is another compound which, according to our tracer studies, interferes with transmembrane Ca uptake into the myocardium. As expected the rat hearts were also protected by Vascoril against isoproterenol-induced metabolic disorders and structural alterations. Equiprotective subcutaneous doses, as studied on the right ventricular myocardium of rats, were 600 mg/kg Vascoril, 250 mg/kg prenylamine, 17 mg/kg verapamil or 10 mg/kg D 600.

Restriction of isoproterenol-induced myocardial Ca uptake and necrotization in rats by a new Ca-antagonistic compound (ethyl-4-(3,4,5-trimethoxycinnamoyl) piperazinyl acetate (Vascordil)).

In vorausgegangenen Untersuchungen von Hein, Fleckenstein, Janke, Eckardt und Ludin (1972) wurde daruber berichtet, das es bei der experi­mentellen Linksherz-Hypertrophie der Ratte nach Coarctation der Aorta zu einer auffalligen Einschrankung der β-adrenergen Myokardreaktionen kommt Die physiologische Grundwirkung β-adrenerger Catecholamine -­insbesondere von Isoproterenol — besteht bekanntlich am Ventrikelmyokard in einer Erhohung des transmembranaren Ca++-Einstroms. Hierdurch wird die Ca++-abhangige Myofibrillen-ATPase starker aktiviert und die ATP-Spaltung im kontraktilen System gesteigert. Hieraus resultiert dann die bekannte positiv inotrope Catecholamin-Wirkung. Am hypertrophierten Rattenherzen waren dagegen alle diese β-adrenergen Effekte stark abge­schwacht. So konnte gezeigt werden, das die Radiokalzium-Nettoaufnahme in normale Kontroll-Herzen durch 1 mg Isoproterenol/kg um den Faktor 4 gesteigert werden kann. Injiziert man jedoch die gleiche Isoproterenol-Dosis den Tieren 3 Wochen nach der Aortenkonstriktion, so wird der Radiokalzium-Einbau in das hypertrophierte linke Ventrikelmyokard nur noch geringfugig erhoht. Dabei schien die Einschrankung der β-adrenergen Sti mulierbarkeit mit der Entwicklung des Hypertrophie-Grades quantitativ korreliert zu sein. Je groser das Herz, desto geringer war die mit Radiokalzium quantifizierte β-adrenerge Reaktivitat.

Einschränkung β-adrenerger Myokardreaktionen (45Ca-Aufnahme, ATP-Utilisation) bei Isoproterenol-induzierter Cardiomegalie

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Prevention of myocardial Ca overload and necrotization by Mg and K salts or acidosis.

Restriction of isoproterenol-induced myocardial Ca uptake and necrotization in rats by a new Ca-antagonistic compound (ethyl-4-(3,4,5-trimethoxycinnamoyl) piperazinyl acetate (Vascordil)).

Einschränkung β-adrenerger Myokardreaktionen (45Ca-Aufnahme, ATP-Utilisation) bei Isoproterenol-induzierter Cardiomegalie