Role of colour doppler in predicting adverse foetal outcomes in pre-eclampsia & intra-uterine growth retardation (IUGR)

2012 ◽  
Vol 2 (7) ◽  
pp. 343-344
Author(s):  
Dr. Purvi B Shah ◽  
◽  
Dr. Mili V Dodia ◽  
Dr. Aparna V Dodia ◽  
Dr. Apoorva V. Dodia

2018 ◽  
Vol 6 (2) ◽  
pp. 171-176
Author(s):  
N.I. Anand ◽  
◽  
P.S. Punatar ◽  
Henil Mathukiya ◽  
◽  
...  


1992 ◽  
Vol 4 (1) ◽  
pp. 15-36 ◽  
Author(s):  
L Myatt

Pregnancy results in profound physiological changes in the cardiovascular system, yet these changes are completely reversible. It is apparent that vaso-active factors, some as yet probably unidentified, which act as humoral or local autocrine or paracrine regulators of vasular resistance, play a major role in these cardio-vascular changes. This role may be heightened in pregnancy when there has to be a large increase in blood flow to the uterus and placenta while maintaining adequate flow to other vascular beds. Our knowledge of the mechanisms of action of these vaso-active factors and their interactions with each other still remains incomplete. Alterations in synthesis and action of these vaso-active factors may occur in pregnancies associated with pregnancy-induced hypertension, pre-eclampsia or intra-uterine growth retardation. Investigation of such alterations may help to elucidate the roles of vaso-active factors in both normal and pathological situations. The gestational hormones oestrogen and progesterone, are obviously prime candidates as overall regulators of the cardiovascular changes of pregnancy and as agents which alter the synthesis or action of other vaso-active factors. Currently, much attention is being focused on the role of local autocrine or paracrine vaso-active factors which may be produced by the endothelium or by the underlying vascular smooth muscle cells and alterations in their production or action in the hyptertensive disorders of pregnancy. The endothelium forms the largest endocrine organ within the body and so its importance in the mediation of vascular events should not be under-estimated. The principal objective of this review is to examine the roles of these many autocrine and paracrine vaso-active factors during pregnancy and their relation with the overall regulation of the vascular system. Changes which may occur and be involved in the aetiology of pre-eclampsia and growth retardation will also be examined.



2003 ◽  
Vol 371 (1) ◽  
pp. 61-69 ◽  
Author(s):  
Maria L. LANGDOWN ◽  
Mark J. HOLNESS ◽  
Mary C. SUGDEN

Overexpression of the conserved Ca2+-binding proteins calreticulin and calsequestrin impairs cardiac function, leading to premature death. Calreticulin is vital for embryonic development, but also impairs glucocorticoid action. Glucocorticoid overexposure during late fetal life causes intra-uterine growth retardation and programmed hypertension in adulthood. To determine whether intra-uterine growth retardation or programmed hypertension was associated with altered calreticulin or calsequestrin expression, effects of prenatal glucocorticoid overexposure (maternal dexamethasone treatment on days 15—21 of pregnancy) were examined during fetal life and postnatal development until adulthood (24 weeks). Dexamethasone (100 or 200μg/kg of maternal body weight) was administered via osmotic pump. Calreticulin was detected as a 55kDa band and calsequestrin as 55 and 63kDa bands in 21 day fetal hearts. Only the 55kDa calsequestrin band was detected postnatally. Prenatal glucocorticoid overexposure at the higher dose decreased calreticulin protein expression (26%; P<0.05) but increased calsequestrin protein expression, both 55 and 63kDa bands, by 87% (P<0.01) and 78% (P<0.01); only the 55kDa calsequestrin band was increased at the lower dose (66%; P<0.05). Offspring of dams treated at the lower dexamethasone dose were studied further. In control offspring, cardiac calreticulin protein expression declined between 2 and 3 weeks of age, and remained suppressed until adulthood. Cardiac calsequestrin protein expression increased 2-fold between fetal day 21 and postnatal day 1 and continued to increase until adulthood, at which time it was 3.4-fold higher (P<0.001). Prenatal dexamethasone exposure minimally affected postnatal calsequestrin protein expression, but the postnatal decline in calreticulin protein expression was abrogated and calreticulin protein expression in adulthood was 2.2-fold increased (P<0.001) compared with adult controls. In view of the known associations between cardiac calreticulin overexpression and impaired cardiac function, targeted up-regulation of calreticulin may contribute to the increased risk of adult heart disease introduced as a result of prenatal overexposure to glucocorticoids.



2010 ◽  
Vol 36 (1) ◽  
pp. 58-63 ◽  
Author(s):  
V. Soubasi ◽  
S. Petridou ◽  
K. Sarafidis ◽  
Ch. Tsantali ◽  
E. Diamanti ◽  
...  


Life Sciences ◽  
1971 ◽  
Vol 10 (19) ◽  
pp. 1115-1123
Author(s):  
C. Degremont ◽  
J.M. Roux ◽  
E. Swierczewski ◽  
C. Tordet-Caridroit


1988 ◽  
Vol 26 (3) ◽  
pp. 206-210 ◽  
Author(s):  
N.G. Haddad ◽  
F.D. Johnstone ◽  
P.R. Hoskins ◽  
S.E. Chambers ◽  
B.B. Muir ◽  
...  




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