This study demonstrates that hypoxic contracture in isolated heart muscle is driven by energy supply and demand rather than direct intracellular calcium availability.
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Energy modulation warrants preclinical testing in hypoxic injury; leaves open translation beyond isolated animal myocardium.
Further studies on hypoxic contracture are described, using resting and contracting isolated muscle preparations from several species. The effect of temperature, pH, substrate, calcium concentration, osmolality and inotropic interventions was explored. The 'protective' effect of acidosis was not contingent on its negative inotropic influence. No evidence was adduced that hypoxic contracture can be modulated other than by altering energy supply or demand. The study does not discriminate between rigor and rised cytosolic calcium as mechanisms causing hypoxic contracture, but demonstrates that hypoxic contracture is not directly dependent on the availability of intracellular calcium.
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Lewis et al. (1979) studied this question.
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