Digoxin-like immunoreactive substance and sodium-potassium-adenosine triphosphatase inhibition in normal pregnancy: A longitudinal study
Objective: To measure the levels of digoxin-like immunoreactive substance and digitalis-like factor bioactivity as manifested by sodium-potassium-adenosine triphosphatase (ATPase) inhibition throughout pregnancy. Methods: Serum samples were collected from primigravidas in early (15 ± 1.8 weeks), mid...
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Veröffentlicht in: | Obstetrics and gynecology (New York. 1953) 1997-05, Vol.89 (5), p.743-746 |
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Zusammenfassung: | Objective: To measure the levels of digoxin-like immunoreactive substance and digitalis-like factor bioactivity as manifested by sodium-potassium-adenosine triphosphatase (ATPase) inhibition throughout pregnancy.
Methods: Serum samples were collected from primigravidas in early (15 ± 1.8 weeks), mid (26 ± 1.2 weeks), and late (36 ± 1.1 weeks) gestation, as well as at 6 ± 1.1 weeks postpartum (mean ± standard error). Digoxin-like immunoreactive substance levels were determined by radioimmunoassay and digitalis-like factor bioactivity was determined by inhibition of ATPase. Data were analyzed by means of repeated measures analysis of variance.
Results: In 41 women with normal pregnancy outcomes, levels of digoxin-like immunoreactive substance rose progressively and significantly (
P < .001) throughout pregnancy and returned to normal levels postpartum. Inhibition of ATPase activity also rose significantly (
P < .004), but not as dramatically, during pregnancy and remained elevated 6 weeks postpartum.
Conclusion: Although digoxin-like immunoreactive substance levels rise in pregnancy, functional digitalis-like factor activity, as manifested by inhibition of ATPase, does not parallel this rise strictly, implying that digoxin-like immunoreactive substance receptors may be reset during normal pregnancy. The enhanced cardiac performance that occurs in normal pregnancy may be mediated in part by increased digitalis-like factor activity. |
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ISSN: | 0029-7844 1873-233X |
DOI: | 10.1016/S0029-7844(97)00090-2 |