Abstract
The calcium paradox was first mentioned in 1966 by Zimmerman et al. Thereafter gained great interest from the scientific community due to the fact of the absence of calcium ions in heart muscle cells produce damage similar to ischemia-reperfusion. Although not all known mechanisms involved in cellular injury in the calcium paradox intercellular connection maintained only by nexus seems to have a key role in cellular fragmentation. The addition of small concentrations of calcium, calcium channel blockers, and hyponatraemia hypothermia are important to prevent any cellular damage during reperfusion solutions with physiological concentration of calcium.
Highlights
In 1960 Zimmerman et al.[1,2] described massive lysis of cardiomyocytes after administration of cardioplegia solution without calcium followed by reperfusion with saline solution with calcium physiological concentration in isolated rat heart
After nearly 50 years of the discovery of this paradox, this study aims to discuss some harmful effects of calcium paradox in the heart, considering its importance, molecular mechanisms, cellular ultrastructural changes, additive protective or harmful effect when placed in combination with other solutions and some ways to avoid it
The similarities end here, as there is contraction of myocytes in culture, but not cytolysis, whereas in the isolated heart we found mass lysis of the cells
Summary
In 1960 Zimmerman et al.[1,2] described massive lysis of cardiomyocytes after administration of cardioplegia solution without calcium followed by reperfusion with saline solution with calcium physiological concentration in isolated rat heart. Unlike what would be expected, the complete absence of calcium caused the cardiac arrest, and altered the cell membranes of cardiac myocytes, culminating in the reperfusion phase with their necrosis, explaining the term “paradox”[1]. In the following years many researchers have studied possible physiological mechanisms of paradox, culminating.
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