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Fetal blood vessel count increases in compensation of hypoxia in premature placentas

K Kartini, Ahmad A Jusuf, Sri Widia A Jusman, M Ekawati, Ani R Prijanti
Submission date: Tuesday, 01 December 2015
Published date: Friday, 26 February 2016
DOI: http://dx.doi.org/10.18051/UnivMed.2015.v34.35-42

Abstract


BACKGROUND Prematurity refers to live births before 37 weeks of gestation, wherein the baby is born before the body and its organ systems achieve perfect maturity, and this disorder is still a global problem. The high incidence of prematurity is a problem in developing and also in developed countries. Certain conditions accompanying pregnancies like preeclampsia, infection, and placental insufficiency, may trigger uterine hypoxia, causing premature birth. The placental condition is related to the intra-uterine fetal condition. In prolonged placental hypoxia, there occurs a compensatory mechanism, i.e. an increase in placental angiogenesis. This study aimed to evaluate the effect of hypoxia on fetal blood vessel count as compensatory mechanism for tissue hypoxia. METHODS An observational-analytical cross-sectional design using paraffin blocks of conserved premature placentas, comprising 31 samples of hypoxic premature placentas and 28 samples of non-hypoxic premature placentas, selected using non-random consecutive sampling. The samples were made into slides and stained with hematoxylin-eosin for assessment of histological structure, including fetal blood vessel count and integrity, villus conditions, syncytiotrophoblastic nuclear changes, and syncytiotrophoblastic nuclear aggregation. Mann-Whitney test was used to compare the difference of blood vessel count between groups. RESULTS Assessment of histological structure showed a significant increase in fetal blood vessel count in the hypoxic group [8.00 (5-15)] as compared with the non-hypoxic group [7.50 (3-15)]. CONCLUSION The hypoxia in premature placentas caused an increase in the number of fetal blood vessels as a form of compensation for disturbed oxygen homeostasis.

Keywords


Premature; placenta; hypoxia; HIF-1α

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References


World Health Organizatin. MDG 4: reduce child

mortality. Geneva: World Health Organization;

Blencowe H, Cousens S, Chou D, et al. Born too

soon: the global epidemiology of 15 million

preterm births. Reprod Health 2013;10(Suppl

:52:1-14.

World Health Organization. Born too soon: the

global action report on preterm birth. Geneva:

World Health Organization; 2012.

Hutter D, Kingdom J, Jaeggi E. Causes and

mechanisms of intrauterine hypoxia and its

impact on the fetal cardiovascular system: a

review. Int J Pediatr 2010. doi: 10.1155/2010/

Zamudio S, Wu Y, Letta F, et al. Human placental

hypoxia-inducible factor-1α expression

correlates with clinical outcomes in chronic

hypoxia in vivo. Am J Pathol 2007;170:2171-9.

Oladipupo S, Hu S, Kovalski J, et al. VEGF is

essential for hypoxia-inducible factor-mediated

neovascularization but dispensable for

endothelial sprouting. PNAS 2011;108:13264-

Hecht J, Allred E, Kliman H, et al. Histological

characteristics of singleton placentas delivered

before the 28th week of gestation. Pathology 2008;

:372-6.

Mongia SM, Jain SK, Yadav M. Placenta: the

wonder organ. J Indian Acad Forensic Med 2011;

:140-2.

Soni R, Nair S. Study of histological changes in

placenta of anaemic mothers. IOSR-JDMS 2013;

:42-6.

Saga Z, Minhas LA, Rana R. Effects of altitude

on morphology of human placenta with special

reference to terminal vili and syncytial knots.

Int J Pathol 2008;6:26-9.

Biswas S. Placental changes in idiopathic

intrauterine growth restriction. OA Anatomy

;1:1-7.

Majumdar S, Dasgupta H, Bhattacharya A. A

study of placenta in normal and hypertensive

pregnancies. J Anat Soc India 2005;54:34-8.

Salafia C, Popek E. Inflammatory and vascular

placental pathology. Glob Libr Women’s Med

doi: 10.3843/GLOWN.10152.

Kiran N, Zubair A, Khalid H, et al.

Morphometrical analysis of intervillous space

and villus membrane thickness in maternal

anaemia. J Ayub Med Coll Abbottabad 2014;26:

-11.

Carter AM. Maintaining the integrity of

trophoblast during growth of the placenta. Focus

on “insulin-like growth factor I and II regulate

the life cycle of trophoblast in the developing

human placenta”. Am J Physiol Cell Physiol

;294:1303-4.

Bainbridge SA, Belkacemi L, Dickinson M, et

al. Carbon monoxide inhibits hypoxia/

reoxygenation-induced apoptosis and secondary

necrosis in syncytiotrophoblast. Am J Pathol

;169:774-83.

Baergen R. Manual of pathology of the human

placenta. 2nd ed. New York: Springer; 2011.

Belkacemi L, Bainbridge SA, Dickinson M, et

al. Glyceryl trinitrate inhibits hypoxia/

reoxygenation-induced apoptosis in the

syncytiotrophoblast of the human placenta. Am

J Pathol 2007;170:909-20.

Burton G, Jauniaux E. The maternal circulation

and placental shape: villus remodeling induced

through haemodynamics and oxidative and

endoplasmic reticulum stress. In: Burton G,

Barker D, Maffett A, et al, editors. The placenta

and human developmental programming.

Cambridge: Cambridge University Press;2011.

p.161-74.

Nagi A. A monograph placenta examination and

pathology. Biomedica 2011;27:81-99.


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