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Pharmacokinetic properties of the tocolytic agent [Mpa 1 d ‐Tyr(Et) 2 , Thr 4 , Orn 8 ]‐oxytocin (antocin) in healthy volunteers
Author(s) -
Lundin S.,
Broeders A.,
Melin P.
Publication year - 1993
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1993.tb02379.x
Subject(s) - desmopressin , pharmacokinetics , radioimmunoassay , endocrinology , medicine , oxytocin , chemistry , vasopressin , blood sampling , peptide hormone , blood plasma , hormone
Summary OBJECTIVE The aim of this study was to study the pharmacokinetics of antocin, the tocolytic oxytocin antagonist [Mpa 1 d ‐Tyr 2 (Et), Thr 4 , Orn 8 ]‐oxytocin. DESIGN Antocin was injected intravenously as a bolus dose (5 μ mol ). Blood samples were taken at intervals for 240 minutes. In addition, the binding of 125 I‐Tyr 10 ‐antocin to blood constituents was determined and compared with 125 I‐AVP and 125 I‐[Mpa ‐1 d ‐Arg 8 ]‐vasopressin (desmopressin). SUBJECTS Eight healthy, non‐smoking adults, three male and five female. MEASUREMENTS Antocin was measured using a specific radioimmunoassay after prior extraction of the plasma. Plasma binding was estimated using polyethyleneglycol precipitation. RESULTS The rate of plasma disappearance of antocin was best fitted by a biexponential curve. The clearance of antocin was 23.5 ± 7–6 I/h, the volume of distribution was 13.1 ± 3.8 I and the biological half‐life was 39.0 ± 4.1 minutes, A greater proportion of 125 l‐Tyr , 10 ‐antocin bound to plasma proteins (33.5%) and red blood cells (13%) than did 125 I‐AVP, 125 l‐desmopressin and unlabelled desmopressin. CONCLUSIONS The half‐life was longer and the clearance of antocin was less than that found in a previous study when a non‐specific antiserum was used. This is most likely because of the extended blood sampling time period which revealed the biphasic decay pattern. The higher plasma clearance of antocin compared to oxytocin and desmopressin may be explained by its increased binding to blood constituents rather than by differences in enzymatic degradation of the molecules.