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Lack of reactivity of uterine arteries from patients with obstetric hemorrhage

  • Author Footnotes
    1 From the Department of Anesthesiology, The University of Texas Medical Branch.
    Sharon H. Nelson
    Correspondence
    Reprint requests: Sharon H. Nelson, PhD, Department of Anesthesiology, The University of Texas Medical Branch, Galveston, TX 77550.
    Footnotes
    1 From the Department of Anesthesiology, The University of Texas Medical Branch.
    Affiliations
    Galveston, Texas
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  • Author Footnotes
    1 From the Department of Anesthesiology, The University of Texas Medical Branch.
    Maya S. Suresh
    Footnotes
    1 From the Department of Anesthesiology, The University of Texas Medical Branch.
    Affiliations
    Galveston, Texas
    Search for articles by this author
  • Author Footnotes
    1 From the Department of Anesthesiology, The University of Texas Medical Branch.
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      Obstetric hemorrhage may occur throughout pregnancy and the Puerperium. The purpose of this study was to investigate the reactivity of isolated, suffused uterine arteries from obstetric patients with uncontrollable uterine bleeding and to compare those blood vessels with uterine arteries from patients undergoing cesarean hysterectomy for other medical reasons (control patients). The uterine arteries from the control patients (n = 9) responded with maximal or near-maximal constriction to norepinephrine (30 μmol/L, 3.6 ± 1 gm), potassium chloride (75 mmol/L, 10.2 ± 3 gm), prostaglandin F (30 μmol/L, 1.8 ± 1 gm), and arginine vasopressin (1 μmol/L, 18.8 ± 2.6 gm). In uterine arteries from five patients with uncontrollable bleeding, the constrictor responses to the same drugs were markedly depressed: norepinephrine (30 μmol/L, 0.5 ± 0.2 gm), potassium chloride (75 mmol/L, 1.9 ± 0.8 gm); prostaglandin F (30 μmol/L, 0 gm), and arginine vasopressin (1 μmol/L, 0.2 ± 0.05 gm). Uterine arteries from two patients exhibited no constrictor responses to norepinephrine (30 μmol/L), potassium chloride (75 mmol/L), prostaglandin F, (30 μmol/L), or arginine vasopressin (1 (μmol/L). The impaired responses to the vasoconstrictor drugs were not reversed by indomethacin (1 μmol/L), which is an inhibitor of prostaglandin synthetase; methylene blue (10 μmol/L), which is a blocker of endothelium-derived relaxing factor activation of guanylate cyclase; or propranolol (1 μmol/L), a ß-adrenergic receptor antagonist. The levels of adenosine 3′:5′-cyclic monophosphate were not elevated in the uterine arteries from the patients with obstetric hemorrhage. The impaired reactivity to the multiple vasoconstrictors implies that a mechanism involved in constriction common to all of the constrictors is depressed or blocked. Furthermore, the depression or lack of reactivity of these isolated uterine arteries is not mediated by vasodilatory prostaglandins, endothelium-derived relaxing factor, ß-adrenergic receptors, or elevated levels of adenosine 3′:5′-cyclic monophosphate. The results suggest that obstetric hemorrhage involves, in part, a lack of constrictor reactivity of the uterine vasculature.

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