P623Intrauterine growth restriction alters myosin thick filaments ultrastructure in cardiac sarcomeres and persists in adult life

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Recent studies relate intrauterine growth restriction (IUGR) and cardiovascular remodelling occurring in fetal life, reporting that IUGR induces dilated and less efficient hearts. However, data characterizing the effects of adverse uterine conditions caused by IUGR at the level of cardiac sarcomere ultrastructure is scarce. In this study we show that IUGR rabbit fetuses present an altered ultrastructure of cardiac sarcomere thick filaments that persist in adulthood.


IUGR was induced in 10 pregnant New Zealand Rabbits by a standard surgical protocol. Puppies were assigned to: i) fetal (30 days of gestation) or ii) young adult (70 days postnatally) study groups. Fetal cardiac function was assessed by echocardiography. Ultrastructural changes of cardiac sarcomeres were measured by Polarization Second Harmonic and standard computation of Myosin Helical Pitch Angle (Myo-HPA).


Fetal cardiac function of IUGR rabbits was found to be consistent with previous results in IUGR human, showing a compromised systolic and diastolic function. IUGR rabbits showed a significantly increased Myo-HPA at 30 days of gestation (mean Myo-HPA=63.9° and 67.4° for controls and IUGR fetal rabbits, respectively. p=0.047). Increased Myo-HPA persisted in IUGR rabbits at 70 days of age (mean Myo-HPA=68.7° and 71.1° for controls and IUGR young adult rabbits, respectively. p=0.040).


The observed Myo-HPA shift in IUGR subjects is related to an altered status of the ultrastructure of myosin thick filaments in cardiac sarcomeres. Myo-HPA is strongly related to Myosin Heavy Chain, a key molecule in cardiac compliance, and it would provide a direct explanation to the adverse cardiovascular outcome found in fetal IUGR in both humans and rabbits.

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