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Myocardial transcapillary exchange in the hypertrophied heart of the dog
Insights
Pathological hypertrophy in dogs significantly increases myocardial transcapillary exchange of substances like urea and sucrose. Exercise-induced hypertrophy did not alter these exchange rates, suggesting different mechanisms for cardiac enlargement.
Area of Science:
- Cardiovascular Physiology
- Myocardial Biology
Background:
- Cardiac hypertrophy, an enlargement of the heart muscle, can result from physiological (exercise) or pathological (disease) stimuli.
- Understanding how hypertrophy affects the heart's ability to exchange substances across capillaries is crucial for comprehending its functional consequences.
Purpose of the Study:
- To investigate myocardial transcapillary exchange in control, exercise-hypertrophied, and pathologically hypertrophied canine hearts.
- To compare the permeability and surface area characteristics of myocardial capillaries under different hypertrophic conditions.
Main Methods:
- Employed the single-injection indicator diffusion method in intact, working hearts of anesthetized dogs.
- Measured myocardial extractions (E), capillary clearances (C), and permeability surface area products (PS) for urea, sucrose, and inulin.
Main Results:
- Both exercise and pathological hypertrophy reduced coronary vascular resistance.
- Myocardial exchange parameters (E, C, PS) for urea, sucrose, and inulin were not significantly different in exercise-hypertrophied hearts compared to controls.
- Pathologically hypertrophied hearts showed significantly increased myocardial E, C, and PS values compared to controls.
Conclusions:
- Pathological cardiac hypertrophy, unlike exercise-induced hypertrophy, enhances myocardial transcapillary exchange.
- This enhancement may be attributed to an increased capillary pore radius or a doubled capillary surface area available for exchange in pathological hypertrophy.
Abstract:
Myocardial transcapillary exchange was investigated in control hearts and in two types of hypertrophied hearts: exercise hypertrophy and pathological hypertrophy due to tricuspid insufficiency. Using the single-injection indicator diffusion method (6, 28), myocardial extractions (E), capillary clearances (C), and permeability surface area products (PS) of urea, sucrose, and inulin were measured in intact, pump-perfused, working hearts of anesthetized dogs. Both types of cardiac hypertrophy were associated with a decreased coronary vascular resistance. Myocardial E, C, and PS values from the exercised group were not significantly different from control. Dogs with pathological hypertrophy exhibited increased central venous pressures, RVEDP's, and heart rates which were greater than control values. The E, C, and PS values from the pathologically hypertrophied hearts were significantly greater than control. These increases in myocardial transcapillary exchange can be explained either by increasing the equivalent pore radius of myocardial capillary membranes from a control value of 70 to 100 A or by assuming that pathologically hypertrophied hearts have a myocardial capillary surface area available for exchange which is twice that of control hearts.