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C. Legrand and J. P. Maltier

Summary. 6-Hydroxydopamine, when injected at 14:00 h on Days 21 and 22 of pregnancy in the rat (2 × 50 mg/kg), markedly decreased plasma and uterine noradrenaline concentrations ( − 60% and −82% respectively; P < 0·001). As a consequence of this treatment, there was severe disturbance in the distribution pattern of parturitions: 61% of rats had suppressed parturition and 31% of rats displayed a lengthened or interrupted labour. A bolus dose of prazosin (3 mg/kg) administered at 12:00 h on Day 22 completely blocked the normal process of parturition throughout the next 6 h, a result which is compatible with the half-life of the drug (2·9 ± 0·8 h). Administration of phentolamine (3 mg/kg) at term induced a significant decrease of uterine activity (frequency × duration of bursts of spike potentials) as revealed by electromyographic recordings in vivo. These results suggest that noradrenaline released from sympathetic nerve terminals interacts with α-adrenoceptors located post-synaptically to improve the overall excitability of the myometrium at the onset of labour.

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Françoise Cavaillé and J. P. Maltier

Summary. Rats were unilaterally ovariectomized on Day 17 of pregnancy and the times of onset of parturition were recorded. Unilateral ovariectomy did not delay the onset of parturition in bilaterally pregnant rats. In rats which were unilaterally pregnant (spontaneously or after ligation of one uterine horn), removal of the ovary on the side of the gravid horn led to delayed or partial parturitions. When fetuses and placentas were removed from one uterine horn on Day 13 and the ovary from the opposite side on Day 17, or when the uterine artery and/or vein were ligated on one side and the ovary removed from the other, about half of the parturitions were abnormal. It is suggested that a substance produced by the gravid uterine horn is transmitted to the ovary, primarily by a local circulatory system, and thus initiates the onset of parturition.

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C. Legrand, A. Banuelos-Nevarez, and J. P. Maltier

Summary. In the early pregnant rat, electrical activity of the myometrium consisted of regular bursts of spike potential, which appeared well propagated on Day 2 of pregnancy. During Day 3, there was a gradual disappearance of propagated activity. Concomitantly, there was a 7-fold increase (P < 0·001) of uterine progesterone concentrations. At this stage, mean duration of bursts was 15·2 ± 0·9 sec and intervals of complete quiescence between bursts were 84·2 ± 7·0 sec. At 10:00 h on Day 4, there were peaks in the uterine concentrations of oestradiol and progesterone, + 36% and + 654%, respectively, compared with values on Day 2 (P < 0·05). Between 10:00 and 20:00 h on Day 4, EMG activity exhibited a rapid and transient rise: bursts were of longer duration at the utero-tubal end of the horn (+ 60%, P < 0·05) with an increased amplitude of spike potentials (+67% and +90% respectively at the tubal and cervical ends of the uterus, P < 0·05). The administration of prazosin depressed EMG activity reversibly in a dose-dependent manner with maximal inhibition at about 2–3 h later. It is concluded that the changes observed during EMG recordings are relevant to the intrauterine distribution of blastocysts and related to changes in the steroidal environment and/or to catecholamine effects via α1-adrenoceptors.

Keywords: myometrial activity; blastocyst distribution; prazosin; rat

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C. Legrand, A. Banuelos-Nevarez, C. Rigolot, and J. P. Maltier

Summary. Sympathetic nerve terminals were destroyed by administration of 6-hydroxydopamine (2 × 50 mg/kg) at 10:00 h on Days 4 and 5 of pregnancy in the rat. In the myometrium, this treatment markedly decreased noradrenaline concentrations (by 99%, P < 0.001), demonstrating that myometrial noradrenaline is mainly originated from sympathetic nerves; therefore after 6-hydroxydopamine, the distribution and spacing of blastocysts remain unaffected throughout the uterus. Administration of phenoxybenzamine (2 × 6 mg/kg) in the morning of Days 4 and 5, or prazosin (4 × 3 mg/kg) from 12:00 h on Day 4 until 12:00 h on Day 5 disorganized the even distribution of blastocysts from the tubal end to the cervical end of the uterine horns. These results provide evidence that a noradrenergic transmission via action on myometrial post-synaptic α1-adrenoceptors is involved as a regulatory mechanism of uterine motility for distribution and spacing of blastocysts in the rat uterus.