Objective: The aim of this study was to show the effect of erythropoietin on ischemia-reperfusion-induced oxidative damage in fetal rat brain. Methods: Fetal brain ischemia was induced by clamping the utero-ovarian artery bilaterally for 20 min, and reperfusion was achieved by removing the clamps for 30 min. The control group was made up of noninjured rats that were 19 days pregnant. In the ischemia-reperfusion group no treatment was given, while 0.4 ml of human serum albumin solution and 5,000 U/kg recombinant human erythropoietin (r-Hu-EPO) were administered in the vehicle and treatment groups 30 min before ischemia-reperfusion injury. Lipid peroxidation in the brain tissue was determined as the concentration of thiobarbituric acid-reactive substances (TBARS) for each fetal rat. A one-way analysis of variance and the post-hoc test were used for statistical analysis. Results: TBARS increased to statistically significantly higher levels in fetal rat brain after ischemia-reperfusion injury than were found in the control group. Recombinant human erythropoietin prevented the increase in TBARS after ischemia-reperfusion injury. Conclusion: Recombinant human erythropoietin has been shown to have neuroprotective effect in intrauterine ischemia-reperfusion-induced fetal brain damage in rats.

The objective of this paper is to investigate whether Helicobacter pylori is an etiologic factor in hyperemesis gravidarum. Thirty one patients with hyperemesis gravidarum and twenty nine pregnant controls without hyperemesis gravidarum were included in this prospective study. All pregnant women were examined both for Helicobacter pylori serum immunoglobulin G antibodies (HpIgG Ab), showing chronic infection, and Helicobacter pylori stool antigens (HpSA), showing active gastrointestinal colonization. Chi-square and Student t tests were used accordingly for statistical analysis. Helicobacter pylori seropositivity was 67.7% in the patients with hyperemesis gravidarum and 79.3% in the control group (χ2 = 1.02, P = .31). HpSA was detected in 22.6% of patients with hyperemesis gravidarum, whereas 6.9% of patients in the control group. The difference was not statistically significant (χ2 = 2.89, P = .08). In this study, no relation was found between Helicobacter pylori and hyperemesis gravidarum. The low social status of women in both groups could be one of the reasons for the high prevalence of Hp infection.

The purpose of this study was to investigate whether propofol has a neuroprotective effect on the fetal brain after intrauterine ischemia-reperfusion (I/R) injury in the rat fetus. Fetal brain ischemia was induced by clamping the utero-ovarian artery bilaterally for 30 min and reperfusion was achieved by removing the clamps for 2 h. A 40-mg/kg single dose of propofol was administered intraperitoneally 15 min before I/R injury. Lipid peroxidation in the brain tissue was determined as the concentration of thiobarbituric acid reactive substances (TBARS) for each fetal rat. Results showed that lipid peroxidation byproducts increased after I/R injury. Maternal treatment with propofol reduced TBARS compared to the I/R group. Propofol has been shown to have neuroprotective effects in intrauterine I/R-induced fetal brain damage in rats.

Further investigations are needed to understand the mechanism of the hepatoprotective effect of erythropoietin and the clinical importance of ischemic liver injury in the fetus.