These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The effect of prostaglandins and other vasoactive substances on uterine blood flow and myometrial activity.
    Author: Still JG, Greiss FC.
    Journal: Am J Obstet Gynecol; 1978 Jan 01; 130(1):1-8. PubMed ID: 619633.
    Abstract:
    The effects of prostaglandins (PG's), bradykinin, and adenosine on uterine blood flow (UBF) and intrauterine pressure (IUP) were investigated in conscious oophorectomized ewes. PGE1 and adenosine increased UBF to levels comparable to those induced by estradiol-17beta, whereas PGE2 and PGA1 achieved only 20 and 36 per cent of peak estradiol-induced levels, respectively. PGE1, PGE2, and adenosine all caused transient increases in IUP while PGA1 had no effect on myometrial activity. Bradykinin increased UBF to 60 per cent of peak estradiol-induced levels, with concomitant increases in IUP tonus. PGE2 and PGF2alpha decreased peak estrogen-induced UBF by 50 and 70 per cent, respectively, while inducing related increases in IUP. When compared with oxytocin, the effects of PGE2 at high flow appeared to be mediated only my myometrial activity, whereas PGF2alpha apparently caused vasoconstriction as well. These findings support the concept that PGE1 could play a role in mediating estrogen-induced uterine vasodilatation. The effects of prostaglandin E1 (PGE1), PGE2, PGF2a, PGA1, bradykinin, and adenosine on uterine blood flow and intrauterine pressure were compared with that of estradiol-17beta in ovariectomized, estradiol-treated ewes. PGE1 and adenosine increased uterine blood flow, measured with implanted electromagnetic flow probes encircling each uterine artery, to levels comparable to those induced by estradiol, which averaged 116 ml/minute. PGE2, PGA1, and bradykinin increased blood flow 20, 36, and 80% of that caused by estradiol. Adenosine produced a flow comparable to the maximal estradiol response. PGE2 and PGF2a decreased peak estradiol-induced uterine flow 50 and 70%, yet increased uterine pressure. The effects of PGE2 appeared to be mediated by myometrial activity; PGE1 could possibly mediate estrogen-induced uterine vasodilation.
    [Abstract] [Full Text] [Related] [New Search]