Neuroprotective effect of magnesium sulfate treatment on fetal brain in experimental intrauterine ischemia reperfusion injury.

OBJECTIVE: The aim of this study was to demonstrate the neuroprotective effect of magnesium sulfate on ischemia-reperfusion-induced injury in fetal rat brain. METHODS: Twenty-four, 19-days pregnant rats were randomly allocated into four groups. 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 consisted of noninjured rats. No treatment was given in the ischemia-reperfusion group; whereas 1 ml saline and 600 mg/kg magnesium sulfate was administered in the vehicle and the 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 post hoc test were used for statistical analysis. RESULTS: TBARS levels were found to be increased after ischemia reperfusion injury when compared with controls. Magnesium sulfate treatment prevented the increase in TBARS after ischemia reperfusion injury. CONCLUSIONS: We have shown that magnesium sulfate decreases TBARS levels significantly in fetal rat brain subjected to ischemia reperfusion injury and may have potential therapeutic benefits by reducing oxidative stress after intrauterine ischemia-reperfusion-induced fetal brain damage.

The effects of estrogen therapy and estrogen combined with different androgenic progestins on carbohydrate and lipid metabolism in overweight-obese younger postmenopausal women.

OBJECTIVE: The aim of the present study was to compare the effect of three different progestins with differing androgenicity on carbohydrate and lipid metabolism in overweight-obese younger postmenopausal women. Additionally, the relationship between testosterone and insulin resistance was assessed. METHODS: The study included 125 postmenopausal women. Estradiol (E(2)) 2 mg/day was given to 20 hysterectomized women and the remaining 105 women were randomized into three treatment groups: E(2) 2 mg/day plus dienogest 2 mg/day (n=35); E(2) 2 mg/day plus norethisterone acetate (NETA) 1 mg/day (n=35); E(2) 2 mg/day plus medroxyprogesterone acetate (MPA) 2.5 mg/day (n=35). A 75-g oral glucose tolerance test was performed at the initial and 3-month visit. Serum glucose, insulin, total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglycerides were measured before and after treatment. RESULTS: A significant treatment-related increase was observed only in the E(2)/MPA group for insulin resistance (p=0.031). When the change in the insulin/glucose ratio was compared, the E(2) group was significantly different from the E(2)/MPA and E(2)/NETA groups (p=0.008 and 0.02, respectively). Only the E(2)/dienogest group showed a treatment-related increase in fasting glucose level (p=0.037). A decrease in total cholesterol and LDL-C levels was observed in all groups (p=0.004 and 0.012, respectively). The only significant decrease in HDL-C level was observed in the E(2)/NETA group (p=0.005). CONCLUSION: Estrogen therapy had a positive effect on carbohydrate and lipid metabolism in overweight-obese postmenopausal women. The addition of progestin to estrogen therapy attenuated estrogen's positive effects slightly; however, the biological actions of the three different androgenic progestins used did not result in any variation.

Helicobacter pylori seropositivity and stool antigen in patients with hyperemesis gravidarum.

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 (chi(2) = 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 (chi(2) = 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.

Maternal treatment with propofol attenuates lipid peroxidation after transient intrauterine ischemia in the neonatal rat brain.

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.

Erythropoietin prevents ischemia-reperfusion from inducing oxidative damage in fetal rat brain.

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 non-injured 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.