NDLI: Fetal hemodynamic changes and mitochondrial dysfunction in myocardium and brain tissues in response to anemia: a lesson from hemoglobin Bart’s disease

Content Provider	Springer Nature : BioMed Central
Author	Luewan, Suchaya Apaijai, Nattayaporn Chattipakorn, Nipon Chattipakorn, Siriporn C. Tongsong, Theera
Abstract	Objective Whether or not the effects of anemia in the early phase, while the fetuses attempts to increase cardiac output to meet oxygen requirement in peripheral organs, is detrimental to the fetal developing vital organs is little-known. The objective of this is to compare prenatal cardiovascular changes and post-abortal cellular damages in the myocardium as a pumping organ and the brain as a perfused organ between anemic fetuses (using fetal Hb Bart’s disease as a study model) in pre-hydropic phase and non-anemic fetuses. Methods Fetuses affected by Hb Bart’s disease and non-anemic fetuses at 16–22 weeks were recruited to undergo comprehensive fetal echocardiography. Cord blood analysis was used to confirm the definite diagnosis of fetal Hb Bart’s disease and normal fetuses. Fetal cardiac and brain tissues were collected shortly after pregnancy termination for the determination of oxidative stress and mitochondrial function, including mitochondrial ROS production and mitochondrial membrane changes. Results A total of 18 fetuses affected by Hb Bart’s disease and 13 non-anemic fetuses were recruited. The clinical characteristics of both groups were comparable. The affected fetuses showed a significant increase in cardiac dimensions, cardiac function, cardiac output and brain circulation without deteriorating cardiac contractility and preload. However, in the affected fetuses, mitochondrial dysfunction was clearly demonstrated in brain tissues and in the myocardium, as indicated by a significant increase in the membrane potential change (p-value < 0.001), and a significant increase in ROS production in brain tissues, with a trend to increase in myocardium. The findings indicated cellular damage in spite of good clinical compensation. Conclusion The new insight is that, in response to fetal anemia, fetal heart increases in size (dilatation) and function to increase cardiac output and blood flow velocity to provide adequate tissue perfusion, especially brain circulation. However, the myocardium and brain showed a significant increase in mitochondrial dysfunction, suggesting cellular damage secondary to anemic hypoxia. The compensatory increase in circulation could not completely prevent subtle brain and heart damage.
Related Links	https://bmcpregnancychildbirth.biomedcentral.com/counter/pdf/10.1186/s12884-023-06232-x.pdf
Ending Page	9
Page Count	9
Starting Page	1
File Format	HTM / HTML
ISSN	14712393
DOI	10.1186/s12884-023-06232-x
Journal	BMC Pregnancy and Childbirth
Issue Number	1
Volume Number	24
Language	English
Publisher	BioMed Central
Publisher Date	2024-02-16
Access Restriction	Open
Subject Keyword	Reproductive Medicine Maternal and Child Health Gynecology Anemia Brain Fetus Heart Hemodynamics Hemoglobin Bart’s disease
Content Type	Text
Resource Type	Article
Subject	Obstetrics and Gynecology
Journal Impact Factor	2.8/2023
5-Year Journal Impact Factor	3.4/2023

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