Decrease in Wound Tensile Strength Following Post-Surgical Estrogen Replacement Therapy in Ovariectomized Rats During the Early Phase of Healing is Mediated Via ER-α Rather than ER-β: A Preliminary Report
Received 5 November 2008 published online 01 April 2009.
Background
In cases of acute surgery or trauma, the most effective method of increasing the level of estrogen in postmenopausal women is its administration immediately pre- or postsurgery. However, in our previous study (J Surg Res 2008; 147:117-122) we showed that postsurgical administration of nonspecific estrogen receptor (ER) agonist decreases wound tensile strength. Therefore, the aim of this study was to evaluate whether this effect is mediated via the α or β ER.
Materials and Methods
Three months prior to the wound healing experiment, 18 rats were anesthetized and underwent ovariectomy (OVX), while another six rats were sham operated. Two parallel full thickness skin incisions were performed on the back of each rat. Doses of 1mg/kg of either PPT (ER-α agonist) or DPN (ER-β agonist) were administered to 12 OVX rats for 6 d postoperatively, whereas all other animals received vehicle. After 6 d, all animals were sacrificed and samples removed for wound tensile strength measurement and histologic evaluation.
Results
The mean wound tensile strength of PPT-treated rats (6.8±1.9g/mm2) was significantly lower compared with all other groups (P<0.05). No significant differences were observed between DPN-treated (8.9±2.2g/mm2), non-OVX vehicle-treated (8.7±2.0g/mm2), and OVX vehicle-treated (9.1±1.7g/mm2) rats. Nevertheless, no remarkable differences were found between groups during histologic evaluation.
Conclusion
Our results indicate that the wound tensile strength decrease is mediated through the α rather than β ER.
∗Department of Medical Biophysics, Pavol Jozef Šafárik University, Košice, Slovak Republic
†Department of Pathological Anatomy, University of Veterinary Medicine, Košice, Slovak Republic
‡Department of Histology, University of Veterinary Medicine, Košice, Slovak Republic
§Department of Biophysics, Institute of Experimental Physics, Slovak Academy of Sciences, Košice, Slovak Republic
To whom correspondence and reprint requests should be addressed at Department for Biomedical Research, The East-Slovak Institute for Cardiovascular Diseases, Košice, Slovak Republic.
ABSTRACT