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• W2007348055 abstract "Ischemic contracture of the left ventricle (“stone heart”) occurs in the rat heart after a period of global ischemia at 37° C. The time of onset of contracture can be delayed by various interventions that reduce myocardial energy demand, increase myocardial energy supply or reduce cellular calcium influx. Conversely, the time of onset of contracture may be advanced by interventions that reduce the energy supply. Analysis of myocardial energy metabolism, and particularly of adenosine triphosphate (ATP) availability in relation to the onset and duration of contracture suggests that contracture is initiated when the cellular ATP content decreases to approximately 12 μmoles/g dry weight. Furthermore, the progression of contracture is characterized by an acceleration in the rate of ATP degradation and the completion of contracture coincides with the reduction of ATP to 3 to 4 μmoles/g dry weight. The results of this study suggest that the development of ischemic contracture represents the accumulation of rigor complexes arising as a result of an ATP deficiency. These rigor complexes are able to exacerbate the contracture by promoting uncontrolled ATP hydrolysis. Although the development of these complexes and the onset of contracture is calcium-insensitive the results indicate that calcium availability may influence the magnitude of the developed contracture. Ischemic contracture of the left ventricle (“stone heart”) occurs in the rat heart after a period of global ischemia at 37° C. The time of onset of contracture can be delayed by various interventions that reduce myocardial energy demand, increase myocardial energy supply or reduce cellular calcium influx. Conversely, the time of onset of contracture may be advanced by interventions that reduce the energy supply. Analysis of myocardial energy metabolism, and particularly of adenosine triphosphate (ATP) availability in relation to the onset and duration of contracture suggests that contracture is initiated when the cellular ATP content decreases to approximately 12 μmoles/g dry weight. Furthermore, the progression of contracture is characterized by an acceleration in the rate of ATP degradation and the completion of contracture coincides with the reduction of ATP to 3 to 4 μmoles/g dry weight. The results of this study suggest that the development of ischemic contracture represents the accumulation of rigor complexes arising as a result of an ATP deficiency. These rigor complexes are able to exacerbate the contracture by promoting uncontrolled ATP hydrolysis. Although the development of these complexes and the onset of contracture is calcium-insensitive the results indicate that calcium availability may influence the magnitude of the developed contracture." @default.
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• W2007348055 title "Ischemic contracture of the myocardium: Mechanisms and prevention" @default.
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• W2007348055 doi "https://doi.org/10.1016/s0002-9149(77)80212-9" @default.
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