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Cytosolic calcium transients in myocytes isolated from rats with ischemic heart failure
1Department of Medicine, New York Medical College, Valhalla 10595.
Insights
Ischemic heart failure impairs cardiac myocyte contractility and alters calcium handling. These cellular changes, including increased diastolic calcium and prolonged calcium transients, contribute to the mechanical dysfunction observed in heart failure.
Area of Science:
- Cardiology
- Cellular Biology
- Physiology
Background:
- Ischemic heart failure significantly impacts cardiac mechanical function.
- Understanding the cellular basis of heart failure is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the mechanical performance and cytosolic calcium (Ca2+) dynamics in myocytes from rats with experimentally induced ischemic heart failure.
- To correlate changes in Ca2+ handling with myocyte mechanical dysfunction.
Main Methods:
- Isolation of myocytes from left and right ventricles of rats subjected to coronary artery narrowing (CAN).
- Characterization of myocyte mechanical properties, including shortening and velocity of shortening.
- Measurement of cytosolic Ca2+ transients, including diastolic and peak systolic Ca2+ levels, and their time courses.
Main Results:
- CAN induced elevated filling pressures and depressed systolic pressures and ejection fraction.
- Myocytes from CAN rats exhibited increased cell dimensions and reduced contractility (myocyte shortening, velocity of shortening).
- Diastolic Ca2+ levels were elevated, while peak systolic Ca2+ was depressed in left ventricular myocytes. Prolonged time to peak Ca2+ and delayed Ca2+ reuptake were observed.
Conclusions:
- Ischemic heart failure is associated with impaired myocyte contractility.
- Alterations in cytosolic Ca2+ handling, particularly elevated diastolic Ca2+ and prolonged Ca2+ transients, contribute to the cellular basis of heart failure.
- These findings highlight the critical role of Ca2+ dysregulation in the pathophysiology of ischemic heart failure.
Abstract:
Mechanical performance and cytosolic Ca2+ dynamics were characterized in myocytes isolated from left and right ventricles of rats with ischemic heart failure. Seven days after coronary artery narrowing (CAN) in rats filling pressures were elevated, whereas systolic pressures and ejection of blood were depressed. Left ventricular myocytes increased 18% in length and 19% in width, whereas right myocytes expanded longitudinally by 23% and transversely by 24%. Contractile behavior of myocytes displayed reductions in myocyte shortening and velocity of shortening, despite prolongation of time to peak shortening. Diastolic Ca2+ increased by 32 and 39% in left and right myocytes of CAN animals, whereas peak systolic Ca2+ in left ventricular myocytes was depressed (22%). Time to peak Ca2+ was prolonged by 68% in left myocytes. Moreover, time required for peak Ca2+ to return to diastolic levels was prolonged in left myocytes. Regression analysis revealed correlations between end-diastolic pressure and diastolic Ca2+ and peak developed pressure and systolic Ca2+. Thus ischemic heart failure finds its cellular basis in a depression in myocyte contractility that may in turn be due to alterations in cytosolic Ca2+ handling.