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Introduction: It was retrospective analysis of prenatal echocardiography findings in fetuses with congenital heart defects, who died in our institution and had an autopsy exams in years 2010 - 2015. Material and methods: Among total 115 deaths the pulmonary hypertension based on histopathology criteria was present in 83 cases (72%) as a leading cause of their deaths. Out of 83 neonates 40 underwent prenatal echo, 43 did not, however in both groups there were similar types of heart defects. Results: The prenatal echo findings from study group (n=40), from the last echo before the delivery were compared with control group and group of HLHS who did survive neonatal surgery and were discharged from hospital. There were statistical differences between pulmonary artery/aorta ratio in fetuses in control group and fetuses in study group („pulmonary hypertension” after birth) (p=0,044). There were statistical differences between pre-delivery pulmonary artery/aorta ratio in fetuses in study group (with „pulmonary hypertension” after birth) and in group of fetuses with HLHS, alive & well after first surgery (p=0,027). There were no differences between pulmonary artery/ aorta ratio fetuses in control group and fetuses with HLHS, alive & well after first surgery (p=0,38) Conclusion: 1) Pulmonary hypertension was a frequent cause of neonatal deaths among our series of congenital heart defects 2) Dilatation of pulmonary artery (and increased pulmonary/artery ratio ) in fetal echo just before delivery may be an important risk factor for poor neonatal outcome in congenital heart defects.)
EN
Apelin (AP) and leptin (LEP) are adipokines with vasomotor actions. Taking into account the published data on the role of obesity in the development of pulmonary hypertension, we studied the implications of apelin on leptin relaxing effects on isolated rat pulmonary arteries. LEP had vasodilatatory effects on phenylephrine-precontracted rat pulmonary arteries from normal and ovalbumin-sensitized rats, but not on rats with monocrotaline-induced pulmonary hypertension. AP13 pretreatment increased LEP effects by one-half. Our studies revealed the existence of synergistic favorable effects of these adipokines on pulmonary vessels.
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