IMR Press / CEOG / Volume 33 / Issue 3 / pii/2006044

Clinical and Experimental Obstetrics & Gynecology (CEOG) is published by IMR Press from Volume 47 Issue 1 (2020). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with S.O.G.

Original Research

A study on the etiology of uterine pressure rise on semen deposition in the vagina or uterus

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1 Department of Surgery and Experimental Research, Faculty of Medicine, Cairo University, Cairo (Egypt)
Clin. Exp. Obstet. Gynecol. 2006, 33(3), 174–177;
Published: 10 September 2006
Abstract

Purpose of investigation: In a recent study we have demonstrated that semen deposition into the vagina or uterus effects uterine pressure rise which is suggested to assist in "sucking" semen into the uterine cavity. The purpose of this study was to investigate whether the uterine pressure rise is effected by the sperm or the substances contained in the seminal plasma, and to test the response of the vagina and uterus to abnormal semen deposition. Methods: Semen was obtained from 60 men divided into four groups: A) obstructive azoospermia, B) Sertoli cell-only syndrome, C) oligozoospermia and D), fertile subjects. Before and after semen deposition into the vagina and uterus both vaginal and uterine pressure were recorded. Results: Semen from groups A and B produced no significant vaginal or uterine pressure changes (p > 0.05) when it was deposited into either the vagina or uterus. Group C and D semen when placed in the vagina or uterus separately effected significant intrauterine pressure rise (p < 0.05) but no vaginal pressure changes (p > 0.05). The pressure rise was higher when the semen was deposited in the uterus than in the vagina (p < 0.05) and with the normospermic than oligozoospermic semen (p < 0.05). In groups C and D, the seminal plasma produced no vaginal or uterine pressure changes (p > 0.05), whereas the sperm effected intrauterine pressurerise (p < 0.05) which was more elevated with sperm from normospermic than oligozoospermic semen (p < 0.05). Conclusions: Aspermic semen did not effect vaginal or uterine pressure rise, while oligozoospermic and normosperm1c semen produced rise of uterine but not vaginal pressure. Uterine pressure rise was induced by the sperm and not the seminal plasma. Further studies are required to define the sulstances secreted by the sperm which produce this increased uterine pressure.

Keywords
Azoospermia
Oligozoospermia
Semen
Sperm
Spermatozoa
Infertility
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