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J Surg Res. 2010 Mar;159(1):e25-8. doi: 10.1016/j.jss.2009.02.024. Epub 2009 Mar 31.

Decrease in wound tensile strength following post-surgical estrogen replacement therapy in ovariectomized rats during the early phase of healing is mediated via ER-alpha rather than ER-beta: a preliminary report.

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1
Department of Medical Biophysics, Pavol Jozef Safárik University, Kosice, Slovak Republic. galovci@yahoo.com

Abstract

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 alpha or beta 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-alpha agonist) or DPN (ER-beta 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+/-1.9 g/mm2) was significantly lower compared with all other groups (P<0.05). No significant differences were observed between DPN-treated (8.9+/-2.2 g/mm2), non-OVX vehicle-treated (8.7+/-2.0 g/mm2), and OVX vehicle-treated (9.1+/-1.7 g/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 alpha rather than beta ER.

PMID:
19592035
DOI:
10.1016/j.jss.2009.02.024
[Indexed for MEDLINE]
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