Abstract
When myocardial cells are reoxygenated after a prolonged period of energy depletion, they rapidly hypercontract. In tissue, hypercontracture induced by reoxygenation is accompanied by cytolysis ("oxygen paradox"). Recent studies have indicated that severe cytosolic Ca2+ overload and reactivation of energy production represent the causal key factors for the deleterious hypercontracture, through the following mechanism: prolonged energy depletion leads to a progressive cytosolic Ca2+ overload in cardiomyocytes; when oxidative phosphorylation is then resumed with the resupply of oxygen, activation of the myofibrils at (still) increased cytosolic Ca2+ concentrations provokes a sustained maximal force development and consecutive mechanical cell injury. This injury can largely be prevented when the contractile machinery is inhibited during the initial phase of reoxygenation. In the model of isolated cells it has been shown that a normal cytosolic Ca2+ control can be reestablished upon reoxygenation. This seems to explain why contractile blockade is needed only temporarily for the prevention of reoxygenation induced hypercontracture and cellular deterioration. Temporary contractile blockade at the onset of reperfusion has also been shown to protect the heart in vivo against lethal reperfusion injury.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
