Key result
Zinc (0.001–5 mm) depressed the contractions of all tested animal cardiac muscle preparations, causing a negative inotropic response and mechanical arrest at concentrations >0.5 mm.
Zinc exerts a negative inotropic effect on cardiac muscle and prolongs the action potential, differing from its known effects on skeletal muscle.
Zinc cardiotoxicity signals in animal models warrant in vivo safety checks; leaves open human myocardial relevance and supplementation risks.
The effect of 0.001–5 mm Zn++ on the contractions of dog, rabbit, and monkey papillary muscles, rat atria, isolated rat hearts, and toad and tortoise ventricular muscle was investigated. Zn++ depressed the contractions of all cardiac muscle preparations tested; the negative inotropic response was associated with an unchanged duration of contraction and a prolonged action potential. Zn++ > 0.5 mm caused mechanical arrest; perfusion of Zn++-arrested amphibian preparations with 100 mm K+ solution resulted in contractures equal in magnitude to that evoked by similar perfusion with 100 mm K+ in the absence of Zn++. It is concluded that the action of Zn++ on cardiac muscle differs essentially from that described for skeletal muscle.
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Nayler et al. (1965) studied this question. Zinc (Zn++) was evaluated on Cardiac muscle contraction. Zinc (0.001–5 mm) depressed the contractions of all tested animal cardiac muscle preparations, causing a negative inotropic response and mechanical arrest at concentrations >0.5 mm.
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