estradiol-3-benzoate and Necrosis

It has been shown that estrogens have a protective effect with regard to tissue ischemia. Therefore, in this macroscopic and histological investigation, the effect of estradiol benzoate on skin flap viability was studied in sham-operated and ovariectomized Sprague-Dawley rats.. Three months prior to flap surgery a group of rats underwent ovariectomy, while the remaining animals underwent a sham operation. Subsequently, all rats had a 2 × 8-cm skin flap created on the dorsum. Rats were randomly divided into estradiol- or saline-treated groups. Treatment started either on the day of flap excision or 3 days prior to the surgery.. Our results showed that administration of estradiol benzoate prior to and after flap surgery significantly decreases skin flap necrosis in both sham-operated and ovariectomized rats, with the highest survival rate in animals where treatment started 3 days prior to flap surgery.. In conclusion, the observed protective effect of estradiol on skin flap viability could potentially be applied to plastic and reconstructive surgery in postmenopausal women. Nevertheless, further research is needed to explain the exact underlying mechanism and to find the optimal treatment protocol for human clinical practice.

Topics: Animals; Disease Models, Animal; Estradiol; Estrogen Replacement Therapy; Female; Necrosis; Ovariectomy; Rats; Rats, Sprague-Dawley; Surgical Flaps; Tissue Survival; Wound Healing

We examined the sequential histopathological changes in the placenta from rats exposed to estrogen. 17 β-estrogiol-3-benzoate was intraperitoneally administered at 100 μg/animal/day during GD 6 to GD 8 (GD6-8 treated group), GD 9 to GD 11 (GD9-11 treated group) and GD 12 to GD 14 (GD12-14 treated group), and the placentas were sampled on GDs 11, 13, 15, 17, and 21. Fetal mortality rates were increased up to approximately 50% in the GD6-8 and 9-11 treated groups, but there was no change of fetal weight on GD 21. An increase in placental weight and a reduction in fetal/placental weight ratio were detected during GD 17 to GD 21 in the GD6-8 treated group. Histopathologically, hypoplasia of metrial gland was detected with defective development of spiral arteries in the GD6-8 and GD9-11 treated groups. A decrease in the thickness of metrial gland was observed from GD 11 onwards in the GD6-8 treated group and from GD 13 onwards in the GD9-11 treated group. The endovascular trophoblasts invaded into the spiral arteries in the deep part of metrial gland in these treated groups. The number of phospho-histone H3 positive cells was decreased on GD 11 or GD 13 in these groups. In the decidua basalis, transitory necrosis was observed with hemorrhage on GD 13 in the GD6-8 and GD9-11 treated groups. In the labyrinth zone, cystic dilatation of the sinusoid was observed with congestion in the GD6-8 treated group, resulting in an increased placental weight. Therefore, we consider that estrogen inhibits the proliferation of decidualized endometrial stromal cells in the metrial gland, and leads to metrial gland hypoplasia with less development of the spiral arteries. The reduced utero-placental blood flow is supposed to be one of the important factors for poor reproductive performance.

Topics: Animals; Cell Proliferation; Estradiol; Female; Fetal Death; Fetal Weight; Gestational Age; Necrosis; Organ Size; Placenta; Placentation; Pregnancy; Rats; Rats, Inbred Strains