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[Depression of contractile function and decrease of the effectiveness of oxygen utilization during compensatory heart
Insights
Heart hypertrophy impairs cardiac function and oxygen use efficiency. This study suggests increased myoplasmic calcium due to impaired calcium pumps causes these changes in hypertrophied hearts.
Area of Science:
- Cardiovascular Physiology
- Cardiac Hypertrophy
- Mitochondrial Function
Context:
- Coarctation of the aorta in rats induces significant heart hypertrophy over 4 months.
- This model allows for the investigation of functional and metabolic changes in the hypertrophied heart.
- Previous research indicates altered energy metabolism in cardiac hypertrophy.
Purpose:
- To investigate the contractile function and oxygen consumption in isolated working hearts with experimentally induced hypertrophy.
- To determine the efficacy of oxygen utilization per unit of function in hypertrophied hearts.
- To explore the underlying mechanisms, specifically the role of calcium handling, in altered cardiac energetics during hypertrophy.
Summary:
- Hypertrophied rat hearts exhibited significantly reduced contractile function compared to controls.
- Oxygen consumption remained unchanged, but oxygen utilization efficacy decreased.
- Glycogen re-synthesis and glycolysis were accelerated, suggesting altered energy substrate utilization.
- A postulated mechanism involves increased myoplasmic calcium due to reduced sarcoplasmic reticulum calcium pump capacity.
Impact:
- Provides insights into the bioenergetic dysfunction accompanying cardiac hypertrophy.
- Highlights the potential role of calcium dysregulation in the reduced efficiency of hypertrophied hearts.
- Suggests potential therapeutic targets related to calcium handling and energy metabolism in heart failure.
Abstract:
Heart hypertrophy was produced in rats by creating a coarctation of the aorta 4 months prior to the experiment. The conducted study of the contractile function and oxygen consumption in isolated working hearts demonstrated a marked decrease in the contractile function of the hypertrophied hearts, as compared to the intact ones. Oxygen utilization, however, remained in these preparations equal to that in the controls: hence, the efficacy of oxygen utilization per unit of function was decreased. At the same time, the process of mobilization--glycogen re-synthesis--is highly activated, and glycolysis--accelerated. In order to explain these phenomena it was postulated that the falling efficacy of oxygen utilization and glycogenolysis activation may be caused by a growing calcium concentration in the myoplasm due to the progressive decrease of the capacity of the calcium pump of the sarcoplasmatic reticulum in the process of heart hypertrophy development.