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Developmental increases in myocardial contractility are driven by changes in intracellular calcium handling, myofibrillar content, and ATPase activity.
This study investigates the developmental changes in myocardial mechanical function and the function of subcellular organelles. Mechanical function was determined at various Ca2+ concentrations ( [Ca2+]0) in the isolated, arterially perfused heart of the fetus (28th day of gestation), newborn (3-5 day old), and adult rabbit. Maximal force of contraction in the fetus (observed at 7.5 mM [Ca2+]0) was significantly less than that in the newborn (observed at 30 mM ( [Ca2+]0), and both the fetus and newborn values were significantly less than that in the adult (observed at 15 mM [Ca2+]0). The myofibrillar content in the fetus and ATPase activity in the fetus and newborn were significantly less than in the adult at pCa 4 and 5 where this enzyme was maximally activated. Both the amount of sarcoplasmic reticulum (SR) and SR Ca2+ uptake per gram of muscle increased with age. Mitochondrial Ca2+ uptake was not observed at pCa more than 6 (physiological range) in all age groups. At pCa less than 6, mitochondrial Ca2+ uptake (per g muscle) in the newborn was significantly greater than in the fetus and adult. Ca2+ uptake by crude homogenate in the newborn was also greater than in the fetus and adult. These data suggest that the age-related change in myocardial contractility is due to the differences in intracellular Ca2+ concentration and myofibrillar content as well as ATPase activity. Intracellular Ca2+ concentration may vary with development depending on the relative capability of Ca2+-releasing system and Ca2+-sequestering system.
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Nakanishi et al. (1984) studied this question.
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