Doppler investigation of uteroplacental blood flow resistance in the second trimester: a screening study for pre-eclampsia and intrauterine growth retardation

1991 ◽  
Vol 98 (9) ◽  
pp. 871-879 ◽  
Author(s):  
SUSAN BEWLEY ◽  
DEREK COOPER ◽  
STUART CAMPBELL
Keyword(s):  
Blood Flow ◽  
Growth Retardation ◽  
Flow Resistance ◽  
Intrauterine Growth Retardation ◽  
Second Trimester ◽  
Intrauterine Growth ◽  
Screening Study ◽  
Uteroplacental Blood Flow

Intrauterine Growth Retardation: Adaptation or Pathology?

PEDIATRICS ◽  
1985 ◽  
Vol 76 (6) ◽  
pp. 998-999
Author(s):  
JOSEPH B. WARSHAW
Keyword(s):  
Blood Flow ◽  
Birth Weight ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Normal Development ◽  
Genetic Influences ◽  
Brain Growth ◽  
Maternal Malnutrition ◽  
Intrauterine Growth ◽  
Uteroplacental Blood Flow

Intrauterine growth retardation can result from a variety of environmental or genetic influences on fetal growth.1 The sequelae of intrauterine growth retardation resulting from impairment of nutrient flow from mother to fetus are well known and include low birth weight with sparing of brain growth, polycythemia, and hypoglycemia resulting from decreased storage fuels and defective gluconeogenesis. Despite the generally held assumption that nutritionally related intrauterine growth retardation (either maternal malnutrition or impaired uteroplacental blood flow) represents a serious pathologic insult to the fetus, the available data suggest that the vast majority of infants with intrauterine growth retardation have normal development without significant differences in IQ or neurologic scores from normal infants.2

DOPPLER ULTRASOUND MONITORING OF FETAL BLOOD FLOW IN CASES OF INTRAUTERINE GROWTH RETARDATION

1994 ◽  
Vol 22 (s1) ◽  
pp. 58-64
Author(s):  
L. Vispi ◽  
P. Vezzosi ◽  
M. Paolieri ◽  
M.G. Gatti ◽  
F. Bagnoli ◽  
...  
Keyword(s):  
Blood Flow ◽  
Doppler Ultrasound ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Fetal Blood ◽  
Intrauterine Growth ◽  
Ultrasound Monitoring

Increased lipolysis but diminished gene expression of lipases in subcutaneous adipose tissue of healthy young males with intrauterine growth retardation

2011 ◽  
Vol 111 (6) ◽  
pp. 1863-1870 ◽  
Author(s):  
Lise Højbjerre ◽  
Amra C. Alibegovic ◽  
Mette P. Sonne ◽  
Flemming Dela ◽  
Allan Vaag ◽  
...  
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Mrna Expression ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Bed Rest ◽  
Whole Body ◽  
Intrauterine Growth ◽  
Glucose Clamp Technique

Intrauterine growth retardation (IUGR) is associated with a central fat distribution and risk of developing type 2 diabetes in adults when exposed to a sedentary Western lifestyle. Increased lipolysis is an early defect of metabolism in IUGR subjects, but the sites and molecular mechanisms involved are unknown. Twenty IUGR and 20 control (CON) subjects, aged 20–30 years, were studied before and after 10 days of bed rest using the glucose clamp technique combined with measurements of in vivo metabolism by microdialysis technique and blood flow by 133Xe washout technique in subcutaneous abdominal (SCAAT) and femoral (SCFAT) adipose tissue. Additionally, mRNA expression of lipases was evaluated in biopsies from SCAAT. Lipolysis in SCAAT was substantially higher in IUGR than in CON subjects despite markedly lower mRNA expression of lipases. Blood flow was higher in IUGR compared with CON in both SCAAT and SCFAT. Whole body insulin sensitivity did not differ between groups and decreased after bed rest. After bed rest, SCAAT lipolysis remained higher in IUGR compared with CON, and SCFAT lipolysis decreased in CON but not in IUGR. Prior to the development of whole body insulin resistance, young men with IUGR are characterized by increased in vivo adipose tissue lipolysis and blood flow with a paradoxically decreased expression of lipases compared with CON, and 10 days of physical inactivity underlined the baseline findings. Subjects with IUGR exhibit primary defects in adipose tissue metabolism.

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