A sizable problem in our understanding of the control of parturition has been a desire by different investigators to explain the whole mechanism in terms of their current theory. We have been offered explanations in terms of factors such as withdrawal of the systemic progesterone block, the local progesterone block, the volume:progesterone ratio, the progesterone:estrogen ratio, the oxytocin effect, the progesterone:oxytocin effect, the fetal role, and the prostaglandin role. With the coming of age of endocrinology and the ability to reduce hormone assays to a routine laboratory service, we have at last begun to understand that many, if not all, rather than anyone of these individual explanations may be implicated in the control of parturition. We now recognize that in late pregnancy a train of events is initiated that ultimately results in the delivery of the fetus. However, we still do not know exactly how and where that train starts, or exactly how it exerts its ultimate action on the myometrial cell. It is a major objective of this chapter to try to bring together some of the abovementioned theories, and particularly to show that, for example, the role of the fetus in the initiation of parturition and the concept of progesterone withdrawal may be part of the same mechanism. It would be folly to say that at the present time either or both of these concepts explain parturition in all species, but by examining a number of different species we hope to illustrate as many of the discrepancies as similarities.

A method has been described for the measurement, by means of Kr 85 , of intrarenal nutrient blood flow distribution in the unanesthetized dog. Injection of the isotope into the renal artery is followed by a multi-exponential disappearance curve which can be obtained by external monitoring with a scintillation detector. In acute experiments autoradiographs have demonstrated that the first exponential component represents cortical blood flow; the second, outer medullary blood flow : the third, inner medullary blood flow; and the fourth, hilar and perirenal fat blood flow. The average cortical blood flow in 65 experiments in five kidneys of four nnanesthetized dogs was 472 ml/100 g/min, the outer medullary 132 ml/100 g/min, and the inner medullary 17 ml/100 g/min. Eighty per cent of the radioactivity was distributed initially to the cortex, 16% to the outer medulla, and 2% to the inner medulla. The hilar and perirenal fat, which receives approximately 2% of the initial radioactivity, was estimated to have a flow rate of 21 ml/100 g/min. In addition, a method for the rapid determination of serial cortical blood flow rates has been described. The importance of these findings has been discussed with reference to the anatomy of the kidney, and to the countercurrent concept as it applies to passive reabsorption of lipid soluble substances, and to the maintenance of an osmotic gradient.

Prolonged pregnancy following foetal hypophysectomy or adrenalectomy (Liggins, Kennedy & Holm, 1967;Drost & Holm, 1968) and premature parturition following injection of corticotrophin or corticosteroids into the ovine foetus (Van Rensburg, 1967;Halliday & Buttle, 1968;Liggins, 1968) implicate the foetal adrenal cortex in the initiation of parturition in sheep. Consequently, foetal plasma corticosteroid concentrations and corticosteroid secretion by the foetal adrenal should be greatly increased towards term. Observations during acute studies on anaesthetized sheep suggest this (Alexander, Britton, James, Nixon, Parker, Wintour & Wright, 1968), but there is no information about blood concentrations or secretion rates of corticosteroids in normal undisturbed sheep foetuses in utero.We cannulated the carotid artery and the facial branch of the jugular vein of four single Merino foetuses with polyvinyl chloride tubing (o.d. 1\m=.\27 mm., i.d. 0\m=.\86mm.) with the ewes under general anaesthesia (pentobarbitone sodium (20 mg./kg., i.v.) followed by halothane and oxygen). The catheters were brought to the exterior through the uterine incision and a separate stab incision in the flank of the ewe. Foetal blood samples (2-3 ml.) were drawn from the carotid catheter daily, followed by a sample from a jugular vein ofthe ewe. Plasma corticosteroid concentrations were determined by the protein-binding method of Bassett & Hinks (1969).One lamb was born after a gestation of normal length and survived ; parturition occurred 8-10 days early in the other three ewes. In these the foetuses were alive at the start of parturition, but two were dead when born.Maternal corticosteroid concentrations were greatly elevated for several days after surgery, but subsequently were generally less than 2 fig.flOO ml. (Fig. 1).Corticosteroid concentrations in the foetal circulation bore little relation to maternal concentrations. Despite the stress of surgery, foetal corticosteroid concentrations were generally below 2 fig./lOO ml. until 130 days gestation. However, commencing several days before birth, there was an increase in the plasma corticosteroid con¬ centration of all the foetuses, unrelated to changes in maternal corticosteroid con¬ centrations (Fig. 1). The highest concentrations, considerably above maternal levels, were reached at the time of birth. In the two lambs which survived birth there was a further temporary increase after birth. Corticosteroid concentrations in all foetuses at birth were similar to those of other newborn lambs (Bassett, Alexande & Oxborrow, 1968). In contrast, no comparable changes in maternal or foetal plasma concentrations of growth hormone, insulin, glucose and fructose or in the percentage oxygen satura-C.S.I.

Renal medullary blood flow was well maintained for several hours after blood loss which produced hypotension. Renal cortical blood flow was altered by trauma and mild hemorrhage even though blood pressure remained normal; rate of blood flow through the subcapsular, peritubular capillaries decreased to the level of that in the outer medulla. With further hemorrhage and the development of hypotension, rate of blood flow in large cortical areas was reduced to that of the outer medulla. With prolonged hypotension, the rate of blood flow in most of the cortex approached outer medullary rate and a single exponential could describe the flow in this combined area. Small regions of even slower flow rate began to appear in the outer cortex; patches of tissue appeared to be completely ischemic. The progression of cortical ischemia noted in these experiments may provide additional evidence for the pathogenesis of the patchy tubular necrosis noted in hemorrhagic shock.