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Dynamics of Pulsatile Prolactin Release during the Postpartum Lactational Period^*

WALLACE C. NUNLEY, RANDALL J. URBAN, JAMES D. KITCHIN, BRUCE G. BATEMAN, WILLIAM S. EVANS and JOHANNES D. VELDHUIS

Interdisciplinary Graduate Biophysics Program (J.D. V.), Departments of Obstetrics and Gynecology (W.C.N., J.D.K., B.G.B., W.S.E., J.D. V.) and Internal Medicine (R.J. V, J.D. V), Biodynamics Institute (W.S.E., J.D.V.), University of Virginia Health Sciences Center Charlottesville, Virginia 22908

Address all correspondence and requests for reprints to: Dr. Johannes D. Veldhuis, Division of Endocrinology and Metabolism, Box 202, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908.

To investigate the pulsatile nature of PRL release in the physiologically hyperprolactinemic postpartum period, we sampled blood at 10-min intervals for 24 h in each of 6 healthy lactating women at both 3 weeks and 3 months postpartum. The subsequent immunoactive PRL time series were subjected to episodic peak detection (Cluster analysis) and multiple parameter deconvolution analysis. The 24-h mean serum PRL concentrations were significantly higher at 3 weeks than at 3 months postpartum; viz. 113 ± 12 vs. 66 ± 15 Mg/L (P = 0.003). Assessment of episodic PRL pulsatility revealed significantly higher maximal PRL peak heights (296 ± 63 vs. 141 ± 44 µg/L), fractional peak heights (863 ± 150 vs. 374 ± 58%), incremental peak amplitudes (250 ± 60 vs. 96 ± 3 µg/L), and peak areas (13 ± 3 vs. 4 ± 1 mg/L·min) in the earlier postpartum period. In contrast, PRL peak frequencies and interpulse intervals were not different in the early and late postpartum sessions. Deconvolution analysis revealed that the mean mass of PRL secretory bursts was significantly greater at 3 weeks (182 ± 4.1 µg/L) than 3 months (15 ± 1.6 µg/L). There were no changes in the calculated half-life of endogenous PRL viz. 29 ± 2.5 min (3 weeks) vs. 26 ± 3.0 min (3 months).

We conclude that physiological postpartum hyperprolactine-mia is achieved by selectively altering the endogenous secretory rate in each PRL release episode, with no change in the number of bursts of PRL discharged or the PRL half-life. (J Clin En-docrinol Metab 71: 287–293, 1991)

^* This work was supported in part by NIH Grant RR-00847 to the Clinical Research Center of the University of Virginia, Research Career Development Award 1KO4-HD-00634 (to J.D.V.), NIH Research Career Development Award 1KO4-HD-00711 (to W.S.E.), Diabetes and Endocrinology Research Center Grant NIH DK-38942, NIH-supported Clinfo Data Reduction Systems, the Pratt Foundation, and the Biodynamics Institute.

Current address: Carolinas Medical Center, Department of Obstetrics (Gynecology), Charlotte, North Carolina 28232.

Received July 18, 1990.

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