Ultrasound probe pressure but not maternal Valsalva maneuver alters Doppler parameters during fetal middle cerebral artery Doppler ultrasonography.

OBJECTIVE: To determine the effects of increased ultrasound probe pressure and maternal Valsalva maneuver (VM) on the middle cerebral artery (MCA) Doppler ultrasonography in fetuses. METHODS: A total of 120 healthy pregnant women in second and third trimesters were enrolled in the study. MCA blood flow was measured by pulsed Doppler sonography in 60 fetuses (24 and 40 weeks' gestation) before and after the application of increased ultrasound probe pressure. In the other 60 fetuses (32 and 36 weeks' gestation), sonography was performed before and after maternal VM. Statistical analysis was performed by paired t-test. RESULTS: The pressure induced by the ultrasound probe induced a significant increase in the pulsatility index (PI), resistance index (RI), and peak systolic velocity (PSV); however, a significant decrease was found in the end-diastolic velocity (EDV) (p < 0.05). No statistically significant difference was found in the mean flow velocity (MFV). Moreover, maternal VM did not have any effect on the PI, RI, EDV, or MFV. CONCLUSION: Fetal MCA Doppler assessment is affected by increased probe pressure but not by maternal VM. Thus, the application of the MCA Doppler sonography should be undertaken in the head of fetuses without any probe pressure and without maternal VM.

Maternal hypoxia increases the susceptibility of adult rat male offspring to high-fat diet-induced nonalcoholic fatty liver disease.

Exposure to an adverse intrauterine environment increases the risk for adult metabolic syndrome. However, the influence of prenatal hypoxia on the risk of fatty liver disease in offspring is unclear. The purpose of the present study was to evaluate the role of reduced fetal oxygen on the development and severity of high-fat (HF) diet-induced nonalcoholic fatty liver disease (NAFLD). Based on design implicating 2 factors, ie, maternal hypoxia (MH) and postnatal HF diet, blood lipid and insulin levels, hepatic histology, and potential molecular targets were evaluated in male Sprague Dawley rat offspring. MH associated with postnatal HF diet caused a significant increase in plasma concentration of triglycerides, free fatty acids, low-density lipoprotein cholesterol, and insulin. Histologically, a more severe form of NAFLD with hepatic inflammation, hepatic resident macrophage infiltration, and progression toward nonalcoholic steatohepatitis was observed. The lipid homeostasis changes and insulin resistance caused by MH plus HF were accompanied by a significant down-regulation of insulin receptor substrate 2 (IRS-2), phosphoinositide-3 kinase p110 catalytic subunit, and protein kinase B. In MH rats, insulin-stimulated IRS-2 and protein kinase B (AKT) phosphorylation were significantly blunted as well as insulin suppression of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase. Meanwhile, a significant up-regulation of lipogenic pathways was noticed, including sterol-regulatory element-binding protein-1 and fatty acid synthase in liver. Our results indicate that maternal hypoxia enhances dysmetabolic liver injury in response to an HF diet. Therefore, the offspring born in the context of maternal hypoxia may require special attention and follow-up to prevent the early development of NAFLD.