The failure of normal mammalian myocardium to maintain tension in high KCl solutions appears to be related to endogenous amounts of catecholamines in the tissue.
Hypothesis-generating for catecholamine modulation of myocardial tension; leaves open relevance to human cardiac physiology.
Contractures induced by KCl are produced in cat ventricular muscle after depletion of catecholamine stores by previous treatment with reserpine or by selective blocking of adrenergic receptor sites with propranalol. Contractures are reproducible for 2 to 3 hours and are markedly depressed by the addition of epinephrine. The relaxation of contracture induced by epinephrine parallels the eftect of this compound of shortening the duration of the normal twitch. The failure of the normal mammalian myocardium to maintain tension in solutions of high KCI concentration appears to be related to the endogenous amounts of catecholamines in the tissue.
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Martin Morad (1969) studied this question.
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