Guinea-pigs were anaesthetized at three stages of pregnancy. Intrauterine pressure was recorded for a 1-h control period and during 10-min intravenous infusions of noradrenaline at rates of 1.0 and 10 micrograms/(min X kg). The mean and maximum amplitude of contractions occurring during the infusions was compared with that of contraction cycles registered in the control period. At 18-21 and 35-43 days post coitum, noradrenaline invariably evoked a rapid and sustained rise in intrauterine pressure, the amplitude of the contractions being greater than during spontaneous contraction cycles recorded in the control period. In late pregnancy, 59-68 days p.c., infusion of 1.0 micrograms noradrenaline/(min X kg) failed to elicit a clear response; contractions occurring during infusion of 10 micrograms noradrenaline/(min X kg) had amplitudes similar to those of the control period and were without a sustained contracture. The absence of denervation hypersensitivity, despite the occurrence of sympathetic denervation in the course of pregnancy, may be due to a generalized effect on excitation-contraction coupling, possibly caused by relaxin.
The effect of acetylcholine upon uteroplacental blood flow was studied by X-ray angiography following selective catheterization of the urogenital artery of the rabbit. Injection of acetylcholine into the artery usually increased the total uterine blood flow. In some cases, this entailed an increase in maternal placental blood flow but, in others, the blood supply to the placenta was cut off and the increased flow passed through the superficial myometrial vessels and, possibly, arteriovenous short circuits. The dichotomy in vascular response depended upon a variation in the myometrial response. In some animals, acetylcholine evoked a large contraction, which curtailed placental flow by compressing blood vessels. In others, the myometrium reacted slightly or not at all to acetylcholine and placental blood flow was able to increase. The vascular and myometrial responses to acetylcholine could be inhibited by previous administration of atropine or butylscopolamine.
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