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Influence of chronic distention on myometrial contractile protein

  • J.W. De Clue
    Footnotes
    Affiliations
    Department of Obstetrics and Gynecology, School of Medicine, University of Missouri Columbia, Missouri, USA

    Department of Physiology, School of Medicine, University of Missouri Columbia, Missouri, USA
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  • G.D. Comfort
    Footnotes
    Affiliations
    Department of Obstetrics and Gynecology, School of Medicine, University of Missouri Columbia, Missouri, USA

    Department of Physiology, School of Medicine, University of Missouri Columbia, Missouri, USA
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  • T.M. King
    Footnotes
    Affiliations
    Department of Obstetrics and Gynecology, School of Medicine, University of Missouri Columbia, Missouri, USA

    Department of Physiology, School of Medicine, University of Missouri Columbia, Missouri, USA
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  • Author Footnotes
    ∗ Submitted in partial fulfillment of the requirement of the Degree of Master of Arts in Physiology, June, 1968.
    ∗∗ Medical Student Research Fellow supported by G.R.S. Grant from the National Institute of Health.
    ∗∗∗ Present address: Department of Obstetrics and Gynecology, Albany Medical College, Albany, New York.
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      Abstract

      Myometrial contractile protein was studied in chronically distended uteri of ovariectomized and estrogen-treated ovariectomized rabbits. Comparative observations were made on uterine surgical specimens obtained from menstruant, postmenopausal, and term pregnant individuals. The animal data indicate that experimentally produced uterine distention does not cause a preferential increase in uterine actomysin. The presence of myometrial hypertrophy resulting in uterine growth is associated with an increase in total myometrial contractile protein. This change in conjunction with an altered viscosity behavior of the isolated actomyosin could account for the increased contractility that has been reported in chronically distended uteri.1
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