OBJECTIVE: To study aspects of the aetiology of primary dysmenorrhoea and mechanisms underlying the therapeutic effect in this condition of an oral contraceptive. INTERVENTION: Intrauterine pressure was recorded before and during infusion of hypertonic saline (5% NaCl, 0.06 ml/kg/min) over 75 min on the first day of bleeding in women with dysmenorrhoea and after 3 weeks of oral contraceptive treatment. Plasma sampling every 15 min of ongoing infusion for the estimation of osmolality, arginine vasopressin, oxytocin and the prostaglandin (PG) F-metabolite, 15-keto-13,14-dihydro-PGF2 alpha. SUBJECTS: Ten healthy nulliparous women with moderate to severe primary dysmenorrhoea. MAIN OUTCOME MEASURES: Plasma levels of posterior pituitary hormones and the PGF-metabolite. Total pressure area (TPA) of the recording curve. RESULTS: In dysmenorrhoea before infusion the plasma concentration of vasopressin was in mean 2.18, oxytocin 5.05 and the PGF-metabolite 321.5 pmol/l, and the TPA 3.8 kPa x 10 min. After oral contraceptive treatment the vasopressin level and the TPA were significantly reduced. At both sessions apart from intensifying the pain, the saline infusion increased vasopressin and oxytocin levels as well as the TPA, whereas the concentration of the PGF-metabolite at both sessions decreased. CONCLUSION: Confirmation is provided of the elevated secretion of arginine vasopressin and PGF2 alpha, as well as increased uterine activity in primary dysmenorrhoea. The observations are in agreement with the concept that a lowered level of vasopressin and a decreased uterine activity contributes to the beneficial effect of OCs in the condition. Stimulation of the secretion of vasopressin increases the uterine activity and symptoms of primary dysmenorrhoea, but results suggest that this effect does not involve a mechanism of increased PGF-synthesis. The role of oxytocin in dysmenorrhoea can not yet be defined.
OBJECTIVE: To study aspects of the aetiology of primary dysmenorrhoea and mechanisms underlying the therapeutic effect in this condition of an oral contraceptive. INTERVENTION: Intrauterine pressure was recorded before and during infusion of hypertonic saline (5% NaCl, 0.06 ml/kg/min) over 75 min on the first day of bleeding in women with dysmenorrhoea and after 3 weeks of oral contraceptive treatment. Plasma sampling every 15 min of ongoing infusion for the estimation of osmolality, arginine vasopressin, oxytocin and the prostaglandin (PG) F-metabolite, 15-keto-13,14-dihydro-PGF2 alpha. SUBJECTS: Ten healthy nulliparous women with moderate to severe primary dysmenorrhoea. MAIN OUTCOME MEASURES: Plasma levels of posterior pituitary hormones and the PGF-metabolite. Total pressure area (TPA) of the recording curve. RESULTS: In dysmenorrhoea before infusion the plasma concentration of vasopressin was in mean 2.18, oxytocin 5.05 and the PGF-metabolite 321.5 pmol/l, and the TPA 3.8 kPa x 10 min. After oral contraceptive treatment the vasopressin level and the TPA were significantly reduced. At both sessions apart from intensifying the pain, the saline infusion increased vasopressin and oxytocin levels as well as the TPA, whereas the concentration of the PGF-metabolite at both sessions decreased. CONCLUSION: Confirmation is provided of the elevated secretion of arginine vasopressin and PGF2 alpha, as well as increased uterine activity in primary dysmenorrhoea. The observations are in agreement with the concept that a lowered level of vasopressin and a decreased uterine activity contributes to the beneficial effect of OCs in the condition. Stimulation of the secretion of vasopressin increases the uterine activity and symptoms of primary dysmenorrhoea, but results suggest that this effect does not involve a mechanism of increased PGF-synthesis. The role of oxytocin in dysmenorrhoea can not yet be defined.