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Utero-placental Circulation (utero-placental + circulation)

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Medical Sciences100%

Selected Abstracts

Placental Anomalies in Children with Infantile Hemangioma

PEDIATRIC DERMATOLOGY, Issue 4 2007
Juan Carlos López Gutiérrez M.D., Ph.D.
We investigated the pathogenic significance of placental features and their relationship to the development of infantile hemangioma in order to obtain a better understanding of its cause. Placental specimens were reviewed from 26 singleton pregnancies of women whose offspring weighed less than 1500 g. A group of 13 neonates who developed infantile hemangioma in the immediate neonate period were compared with 13 healthy preterm infants of comparable postconception age who had no infantile hemangioma. Pathologic placental changes were analyzed in both groups. Gross lesions with disturbance of the utero-placental circulation were found in all placentas from children who developed infantile hemangioma, including massive retroplacental hematoma in two infants, extensive ischemic infarction in seven, and large dilatated vascular communications, severe vasculitis, chorioamnionitis and funiculitis in four. Placental features included percentages greater than 25% of avascular villi, platelet and fibrin aggregates, and multifocal disease involving more than one histologic section. Examination of 13 placentas of low-birth-weight infants without infantile hemangioma only showed abnormal placentation in one and isolated villous dismaturity in two. The higher ratio of placental pathologic findings in patients with infantile hemangioma suggests that reduced placental oxygen diffusive conductance contributes to fetal hypoxic stress and that hypoxic/ischemic changes in the placenta could be related to infantile hemangioma development via vascular endothelial growth factor and placental growth factor expression, among others, within the villious vessels and throphoblasts. [source]

REVIEW ARTICLE: The Contribution of Macrophages to Normal and Pathological Pregnancies

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 6 2010
Takeshi Nagamatsu
Citation Nagamatsu T, Schust DJ. The contribution of macrophages to normal and pathological pregnancies. Am J Reprod Immunol 2010 Macrophages represent one of the major leukocyte subsets in the uterine decidua. Owing to their remarkable phenotypic plasticity, decidual macrophages can participate in diverse activities during pregnancy. At baseline, decidual macrophages are characterized by an immunosuppressive phenotype and M2 polarization, supporting feto-maternal immune tolerance. In early pregnancy, macrophage-derived pro-angiogenic factors prompt vascular remodeling within the uterine wall to ensure appropriate utero-placental circulation. Upon invasion by pathogens, pattern recognition receptors on decidual macrophages help to alter the characteristics of these malleable cells toward an M1, inflammatory phenotype. Similar inflammatory characteristics are seen in those macrophages that accumulate in the lower segment of the uterus to drive cervical ripening. Disturbances in the tight control that balances macrophage function during pregnancy can trigger the development of pregnancy complications. Here, we discuss the physiologic role of uterine macrophages at different stages of pregnancy and describe their relevance in selected pregnancy disorders. [source]

Circulating Endothelial Progenitor Cells During Normal Pregnancy and Pre-Eclampsia

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 2 2006
Keiichi Matsubara
Problem Endothelial progenitor cell (EPC), which mediates neovascularization of uterine endometrium may be involved in the neovascularization in the utero-placental circulation. We evaluated whether EPC proliferation in pre-eclampsia (PE) differed from that in normal pregnancy. Method of study EPC number in peripheral blood (20 non-pregnancy, 36 normal pregnancy, 10 PE) was measured using flow cytometry. Peripheral blood mononuclear cell was cultured for 7 days and EPC proliferation was assessed based on detection of the uptake of acetylated low-density lipoprotein and lectin. Furthermore, the proliferative activity induced by angiotensin II (Ang II) and tumor necrosis factor- , (TNF- ,) was measured by BrdU assay. Results EPC number in peripheral blood did not differ significantly between PE and normal pregnancy; however, EPC proliferation was significantly increased in PE. Furthermore, Ang II and TNF- , induced the proliferation of EPC derived from patients with PE. Conclusions In PE, some factors including Ang II and TNF- , stimulated EPC proliferation; however, the impairment of EPC mobilization into systemic circulation by serum factors may contribute to insufficient regeneration of EC in disturbed utero-placental circulation of PE. [source]