Intramammary Pressure Research Articles

Influence of milk flow rate and streak canal length on new intramammary infection in dairy cows

Eighteen cows with a wide range of quarter peak flow rates (0.35-2.22 kg/min) were inoculated with Streptococcus agalactiae and Str. dysgalactiae 4 mm into each streak canal every 3 d for 12 d. Thirty of the 72 quarters developed intramammary infection. Mean peak flow rate and length of streak canal of those quarters that became infected were 1.26 +/- 0.08 kg/min (mean +/- SEM) and 11.47 +/- 0.41 mm respectively, compared with 1.01 +/- 0.05 kg/min and 12.05 +/- 0.35 mm for those that remained uninfected. Logistic regression analysis showed that the probability of infection increased significantly with the increase in peak flow rate (P = 0.01). The influence of streak canal length on new infection, after allowing for the effect of peak flow rate, was not significant at the 5% level (P = 0.07), suggesting that there may be an inverse relationship between teat duct length and infection, but that it is of secondary importance to peak flow rate. If increased mass of milk distends the teat duct by raising intramammary pressure, then quarter susceptibility to infection is further compromised. These results strongly suggest that the benefits of reduced infection from mastitis control, achieved despite dramatic increases in milk flow rate and milk yield, are significantly underestimated.

Lactational changes in oxytocin release, intramammary pressure and milking characteristics in dairy cows

Two experiments were conducted to investigate possible changes of milking-related oxytocin release (Expt 1) and of intramammary pressure and milking characteristics (Expt 2) throughout entire lactations in German Braunvieh dairy cows. Mean oxytocin concentrations after stimulation at onset of milking increased from 18.3 +/- 15.9 to 30.7 +/- 24.1 pg/ml in Expt 1 and decreased from 23.9 +/- 17.6 to 15.4 +/- 9.1 pg/ml in Expt 2, respectively, but remained above the level necessary to elicit complete milk ejection in both trials. Premilking baseline intramammary pressure had its maximum in early lactation until about month 4 and then decreased to approximately 50% of its initial level. Ejection pressure followed a similar pattern, but dropped only to approximately 75% of its maximum. This was due to the constant elevation of pressure increase, reaching its highest level in late lactation. Time from commencement of stimulation until maximum pressure exceeded 1 min in almost all instances even in early lactation and increased throughout lactation. Despite the normal decrease of milk yield average milk flow fell only slightly while maximum flow rate remained almost constant. Pressure increase, milk yield and milk flow were not different after 1 min and after extended stimulation. Thus there were no indications of a decreasing sensitivity of the milk ejection reflex during lactation, and milking characteristics were positively affected by intense teat stimulation. Suggestions for practical dairying are made.

Measurement of machine-induced changes in thickness of the bovine teat

Machine milking induced repeatable, short-term changes in thickness of the teat apex. These changes were measured with a spring-loaded caliper instrument under milking conditions that imposed differing forces on the teat apex. The mean percentage changes in teat end thickness (relative to the premilking values for individual teats) varied from 10% decrease up to 20% or more increase depending on the particular milking system used. The overall decrease in teat end thickness associated with cannula milking, milking at very low vacuum levels or milking with positive pressure pulsation may result from: (i) decrease in the intramammary pressure; and/or (ii) small changes in tone of teat musculature; and/or (iii) changes in the distribution of interstitial fluids in the teat apex. The overall increase in teat thickness caused by conventional or PKME milking systems results mainly from oedema (the extravascular accumulation of fluid). It is likely that milking equipment can, and should, be designed to minimize circulatory impairment resulting in oedema of the teat.

Facilitatory effect of hypothalamo-neurophypophysial tract stimulation on milk ejection frequency in the lactating rat

The relative contribution of magnocellular and parvocellular neurones to the patterning of milk ejections was studied by activation of various parts of the hypothalamo-neurohypophysial tract. During suckling of anaesthetised lactating rats, electrical stimulation of the neurohypophysis/neural stalk (15 Hz, 1.5 s on 1.5 s off , 10 min) evoked an increased frequency of milk ejections as detected by intramammary pressure recording. Bilateral stimulation of the paraventricular nuclei produced a similar facilitation in the post-stimulus period, but stimulation of the supraoptic nuclei (with either low current or current sufficient to evoke peripheral oxytocin release) had no effect on the occurrence of milk ejections. These data are consistent with the hypothesis that parvocellular but not magnocellular neurones participate in the regulation of milk ejection frequency.

Suppression par la lutectomie de l'accroissement simultané de la pression intramammaire et de l'ocytocinémie, induit par l'injection de PGF2α, chez la brebis

Seven lactating Lacaune ewes underwent either a total luteectomy on day 19 of pregnancy (D19) (compensated from that stage by a daily progesterone supplementation of 25 mg to ensure embryonic survival; group 1:4 animals) or a control laparotomy (group 2: 3 animals). Intra-jugular injection of 200 micrograms of a synthetic PGF2 alpha analogue (Dinolytic, Upjohn) caused an increase in the intramammary pressure (IMP) and a concomitant rise in oxytocinaemia only in the presence of a corpus luteum, ie in all ewes of groups 1 and 2 before D19 and only in those of group 2 after that stage. These experiments confirm that the corpus luteum, and not the other ovarian compartments, releases oxytocin when prostaglandin F2 alpha is administered.

Release of oxytocin within the supraoptic nucleus during the milk ejection reflex in rats.

To investigate the hypothesis that oxytocin may be released within the magnocellular nuclei in vivo, push-pull cannula perfusions were performed in anaesthetized lactating rats in one supraoptic nucleus of the hypothalamus while recording the intramammary pressure and/or the electrical activity of oxytocin cells in the contralateral supraoptic nucleus. Oxytocin content was measured in samples collected over 15 min, under various conditions: 1) with no stimulation; 2) during suckling and suckling-induced reflex milk ejections; 3) during electrical stimulation of the neuro-hypophysis by trains of pulses that mimicked oxytocin cell bursts; 4) under osmotic stimulation by i.p. injection of 2 ml of 1.5 M NaCl to evoke a tonic and sustained oxytocin release from the neurohypophysis. Oxytocin release within the supraoptic nucleus increased significantly during the milk ejection reflex and, to a lesser extent, during burst-like electrical stimulation of the neurohypophysis. In suckled rats, the increase started before the first reflex milk ejection occurred. There was no apparent correlation between the amount of oxytocin in the perfusates and the number of milk ejections and oxytocin cell bursts occurring during each perfusion period. The amount of oxytocin in the perfusates further increased-during facilitation of the milk ejection reflex by intraventricular injections of oxytocin or its analogue, isotocin. When suckling failed to evoke the milk ejection reflex, there was no change in intra-supraoptic oxytocin release. There was also no change after osmotic stimulation. When the push-pull cannula was positioned outside the supraoptic nucleus, there was no increase in the amount of oxytocin during the three types of stimulation tested. These results provide evidence for an endogenous release of oxytocin within the magnocellular nuclei in lactating rats. It is suggested that the increase in such a release induced by suckling is likely to be a prerequisite for the onset and the maintenance of the characteristic intermittent bursting electrical activity of oxytocin cells leading to milk ejections.

Characteristics of milk ejection, associated intramammary pressure changes and oxytocin release in the mare.

The neuroendocrine reflex theory of milk ejection was investigated in the horse under natural suckling conditions. To this end 12 lactating mares were provided with acute jugular catheters and with intramammary pressure (IMP) recording catheters. The foal had free access to the contralateral mammary complex. Intramammary pressure could thus be recorded while blood was drawn simultaneously for oxytocin analysis from the undisturbed animal. Suckling periods associated with a characteristic increase in IMP lasted significantly longer than unsuccessful nursing attempts. Elements of successful sucklings involved physical stimulation of the mammary gland, a quiet phase and a sudden increase in IMP. Successful suckling took place at about 20-min intervals with a wide range from less than 5 min to greater than 100 min. Between 5 and 10 mU oxytocin i.v. were sufficient to evoke an increase in IMP identical in shape and duration to a naturally induced increase in IMP. Mean peak oxytocin levels reached 15.8 pmol/l plasma, with a maximal release of 39 pmol/l. In the majority of cases (greater than 80%) peak oxytocin release did not occur until after the increase in IMP; in some cases an oxytocin surge was not detectable at all, despite a milk ejection-associated increase in IMP. In three cases increase in IMP could be observed while the foals were away from the mother with no signs of any intention to suckle. The data indicate that in the horse some elements of the neuroendocrine reflex, such as tactile stimulation of the teat and a surge of oxytocin before an increase in IMP, are facultative and not essential for normal milk ejection.

Oxytocin release evoked by electrical stimulation of the medial forebrain in the rat: Analysis of stimulus parameters and supraoptic neuronal activity

The role of the medial forebrain area (vertical limb of the diagonal band, medial septum and medial nucleus accumbens) in the control of oxytocin secretion in lactating rats was investigated. Electrical stimulation of the medial forebrain evoked a reproducible rise in intramammary pressure, equivalent to that caused by i.v. injection of 1 mU oxytocin. No presser effect accompanied this response. Radio-immunoassay of plasma samples showed that stimulation caused a significant rise in the concentration of circulating oxytocin. The effects of changing the parameters of stimulation to the medial forebrain were compared with those evoked by stimulation of the neural stalk. The optimal frequency for stimulation of the forebrain was found to be four-fold lower (10–20 Hz) than that for stimulation of the neural stalk (50 Hz). During continuous prolonged stimulation of the forebrain (20 Hz; 2 min) only a single transient response was obtained, whereas a protracted response was obtained as a result of prolonged stimulation of the stalk. Recordings were made from antidromically identified neurosecretory cells in the supraoptic nucleus. Electrophysiological responses to electrical stimulation of the medial forebrain were characterized by two main features. (1) Single-pulse stimulation produced only a small excitation (one or two action potentials), while high-frequency trains produced a profound facilitation of this response, with each pulse evoking short-duration ‘bursting’ behaviour in the supraoptic neurons. (2) During long trains of stimulation this frequency-dependent facilitation declined and could only be renewed after a period of rest. The study indicates that the medial forebrain provides a major excitatory afferent input to the oxytocin-secreting neurons of the supraoptic nucleus, and that the pulse-like secretion of oxytocin following medial forebrain stimulation results from the complex facilitatory and adaptive characteristics of this input.

Inhibition of suckling-induced milk ejections in the lactating rat by delta 9-tetrahydrocannabinol.

The effect of delta 9-tetrahydrocannabinol (THC) on suckling-induced oxytocin release was investigated by recording intramammary pressure changes in suckled rats treated iv with THC (0.5 mg/kg BW) or vehicle. Latency to the first posttreatment milk ejection and posttreatment milk ejection intervals and pressure wave amplitudes were compared between THC- and vehicle-treated rats. Before treatment, intervals between milk ejections averaged 6.5 +/- 1.3 (+/- SE) and 7.0 +/- 0.7 min for vehicle- and THC-treated groups, respectively. Vehicle injections did not alter the frequency of milk ejections, which continued at an overall mean interval of 7.6 +/- 0.7 min after treatment. In contrast, THC treatment was followed by a transient suspension of milk ejections, with a latency of 59.3 +/- 7.4 min before the first posttreatment milk ejection was recorded (P less than 0.001). Intervals between subsequent ejections averaged 15.3 +/- 2.0 to 16.1 +/- 1.3 min and were lengthened relative to corresponding intervals in vehicle-treated animals (P less than 0.05). The amplitudes of pressure waves were not significantly affected by treatment. Oxytocin (0.5 mU) injections 10 or 30 min after THC treatment evoked abrupt increases in intramammary pressure, indicating continued responsiveness of the mammary gland to oxytocin stimulation. These data suggest that THC interferes with the release of oxytocin in response to suckling. To our knowledge, this provides the first evidence that THC inhibits posterior pituitary function.

Naloxone excites oxytocin neurones in the supraoptic nucleus of lactating rats after chronic morphine treatment.

1. Lactating rats were implanted with a cannula in a lateral cerebral ventricle to deliver morphine (up to 50 micrograms/h) chronically from a subcutaneous osmotically driven mini-pump. After infusion of morphine for 5 days the rats were anaesthetized with urethane and prepared with ventral surgery for recording the electrical activity of single, antidromically identified neurones in the supraoptic nucleus. 2. A single I.V. injection of naloxone (5 mg/kg) in these rats provoked a long-lasting, large increase in intramammary pressure, but in control rats had negligible effects. Concentrations in plasma of oxytocin, measured by radioimmunoassay in samples of femoral arterial blood, rose from 44.7 +/- 2.5 to 1072.1 +/- 89.5 pg/ml (means +/- S.E.M.) 6 min after naloxone in the morphine-treated rats. In control rats, the concentration of oxytocin in plasma rose only from 42.1 +/- 2.9 to 125.1 +/- 28.2 pg/ml after naloxone. 3. Naloxone produced a transient increase in arterial blood pressure in morphine-treated but not control rats. Concentrations in plasma of vasopressin, measured by radioimmunoassay in samples of femoral arterial blood, rose in morphine-treated rats from 7.4 +/- 2.4 to 29.2 +/- 3.7 pg/ml after naloxone, but did not rise significantly in control rats. 4. Naloxone (1-5 mg/kg) produced a prompt and prolonged increase in the discharge rate of each of ten continuously active (putative oxytocin) cells recorded from ten morphine-treated rats. The discharge rate of the six cells tested at the highest dose (5 mg/kg) increased by an average of 6.3 Hz (360%) within 5 min, and the firing rate remained elevated for at least 30 min; the discharge rate of six continuously active supraoptic neurones recorded in control rats was not affected by naloxone. 5. The firing activity of five phasic (putative vasopressin) supraoptic neurones in morphine-treated rats was increased for at least 30 min by the injection of naloxone; these increases were the result of a raised intraburst firing rate with no change in burst duration or frequency. One phasic neurone was inhibited for 15 min, and one phasic neurone was unaffected. 6. The excitatory effects of naloxone on neurones in the supraoptic nucleus of morphine-treated rats were not explained by changes in blood pressure or osmolarity and did not depend on suckling or a cholinergic pathway. 7. The concentrations of oxytocin in plasma and the operation of the milk-ejection reflex were similar in the controls and morphine-treated rats, prior to naloxone. These findings indicate tolerance to initial inhibitory effects of morphine on oxytocin secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

PGF2α-induced milk ejection in ewes having cyclic or pregnant corpora lutea

The production of luteal oxytocin in ewes, resulting from the intrajugular injection of 200 micrograms of PGF2 alpha, could be determined by the increase in intramammary pressure. This simple indirect method of measuring the activity of the corpus luteum enabled easy detection of renewed post-partum ovulation or the onset of pregnancy. The response was monitored every two days between Days 0 and 25, then every 4 days between Days 25 and 59 in: 9 cyclic ewes (group B); 9 cyclic ewes treated with three daily intramuscular injections of 25 mg of Trilostane, a steroid synthesis inhibitor, between Days 7 and 25 (group A); 11 pregnant ewes (group C). Progesterone levels were determined each day from blood sampled in the jugular vein. Trilostane produced a decrease in plasma progesterone, not a total suppression (fig. 3), but did not significantly modify the intramammary pressure variations resulting from PGF2 alpha injections. These were identical in both cyclic and pregnant ewes during the first 15 days: they increased from D0 to D7 and decreased between D12 and D15 (fig. 4). After D15, the increase in intramammary pressure progressively weakened and became 0 at D17 in the cyclic ewes, whereas in the pregnant animals there was a renewed increase in intramammary pressure until D20; this regressed progressively afterwards and disappeared towards D45. This transitory, renewed activity between D15 and D20 might be an indirect or direct result of the message delivered by the embryo to maintain the corpus luteum. Several hypotheses are discussed with a view to explaining this phenomenon.

Ejection du lait induite par PGF2α pendant les deux premiers mois qui suivent l'insémination des vaches. Applications à un diagnostic de gravidité

Milk ejection after intrajugular injection of 256 micrograms of a synthetic PGF2 alpha analogue (Dinolytic, Upjohn) was measured every 2 days until D60 in 7 pregnant cows and until D25 in 5 non pregnant inseminated cows (trial 1). There was a very close correlation (r around + 0.98) between the values of the 3 parameters used to characterize milk ejection, i.e. amplitude of intramammary pressure deflection, surface area under the pressure curve, alveolar milk volume collected by a teat probe. In the two groups of animals, these values behaved similarly until D15 with a sudden increase between D2 and D7. From D15 they decreased abruptly in females where insemination had failed while they still remained at a high level until D25 (then decreasing until D60) in those presumed to be pregnant (fig. 2). These responses were assumed to result from the release of luteal oxytocin and it is suggested that a single injection of 256 micrograms of Dinolytic on D20, together with milk ejection control using a teat probe, would be a rapid, little expensive method for the farmer (without risks of luteolysis) (trial 2 and fig. 3) to distinguish between pregnant and non pregnant cows.

Extracellular potassium changes in the rat neurohypophysis during activation of the magnocellular neurosecretory system.

1. Potassium-sensitive microelectrodes were used to measure extracellular [K+] in the isolated rat neurohypophysis maintained in vitro. Electrical stimulation of the neurohypophysial stalk (20 Hz 5 s) increased the inferred extracellular [K+] by 9.2 +/- 0.4 mM (mean +/- S.E. of mean; n = 21). 2. Veratridine (10 microM) enhanced the response to stalk stimulation, and at a higher concentration (50 microM) increased extracellular [K+] in the absence of stimulation. By contrast, tetrodotoxin (1 microM) blocked the [K+] increase completely and reversibly in each of five experiments, indicating that the increase was a consequence of action potential generation. 3. At the end of brief periods of stimulation, the raised extracellular [K+] returned to pre-stimulation levels within 30 s. In the presence of ouabain (100 microM), the recovery was slower: the half-decay time was extended by 150-300% in each of three experiments. 4. Replacement of calcium in the medium with cobalt, cadmium or magnesium reduced the amplitude of the [K+] increase by 26-30%, indicating that the [K+] increase was largely independent of events subsequent to evoked release of hormone and/or transmitters. 5. Potassium-sensitive microelectrodes were placed in the neurohypophysis of rats anaesthetized with urethane. Electrical stimulation of the pituitary stalk (50 Hz, 5 s) produced transient voltage increases of 7.6 +/- 0.9 mV (mean +/- S.E. of mean of seven experiments). These voltage increases were similar in magnitude to the response of the electrodes to the addition of 7.6 +/- 1.0 mM-K+ to rat plasma. 6. In seven lactating rats, the suckling of a litter of hungry pups evoked periodic reflex milk ejections, as detected by increases in intramammary pressure. Potassium-sensitive microelectrodes in the neurohypophysis recorded transient voltage increases prior to each milk ejection (0.4-5.5 mV). Each increase preceded an increase in intramammary pressure by 12-30 s. 7. Thus synchronized high-frequency activation of magnocellular neurones can produce large changes in extracellular [K+]. The implications of these findings for stimulus-secretion coupling in the neurohypophysis are discussed in the light of previous reports that hormone release from the neurohypophysis is highly dependent on the frequency and pattern of electrical stimulation.

The subfornical organ and relaxin-induced inhibition of reflex milk ejection in lactating rats.

Experiments were carried out on anaesthetized, lactating rats to investigate the possible role of the subfornical organ in mediating relaxin-induced inhibition of reflex milk ejection. Milk ejection was judged by the behavioural response of the sucklings and by transient rises in intramammary pressure. Radiofrequency lesions of the subfornical organ, or control lesions in adjacent areas of the cerebrum, did not affect the pattern or the magnitude of intramammary pressure changes at reflex milk ejection. Purified porcine relaxin given by either i.v. (5 micrograms) or intracerebroventricular (50 ng) injection suppressed reflex milk ejection in intact, sham-lesioned and control-lesioned rats, but had no effect on either the pattern or magnitude of reflex milk ejection in rats with lesions of the subfornical organ. The subfornical organ, which is situated at the interface between the blood, brain and the cerebrospinal fluid appears to mediate, at least in part, the relaxin-induced inhibition of reflex milk ejection in the rat.

Effects of chronic infusion of porcine relaxin on oxytocin release in lactating rats.

The effects of chronic infusion of porcine relaxin on oxytocin release were studied in lactating rats. Infusion of relaxin (4.2 micrograms/h for either 4 or 6 days) suppressed reflex milk ejection and reduced litter weight gain for 48 h compared with saline-infused controls. After 2 days, neither the rate of growth nor the frequency of milk ejection were significantly different from controls. For 24 h after the infusion of relaxin ended, litters gained weight more quickly than controls but there was no difference seen in the frequency of milk ejection. The effects on oxytocin release of stopping an infusion of relaxin after 3 days were investigated. There was a significant (P less than 0.01) rise in plasma oxytocin (up to 90 pmol/l) 30 min after the infusion was stopped, followed by a sustained rise in intramammary pressure. Treatment of relaxin-infused rats with naloxone (0.1 mg/kg) when the infusion was halted caused a more rapid release of oxytocin (within 2 min), a greater release of oxytocin (up to 140 pmol/l) and a prolonged rise in intramammary pressure.

Control of magnocellular oxytocin neurones by the region anterior and ventral to the third ventricle (AV3V region) in rats.

The involvement of the region anterior and ventral to the third ventricle (AV3V region) in the control of oxytocin release was investigated using electrical stimulation and electrolytic lesioning techniques in the rat. Electrical stimulation (0.5 mA, 50 Hz, 15-25 s) of the AV3V region of lactating rats evoked a reproducible rise in intramammary pressure equivalent to that induced by 0.25-0.5 mu. oxytocin (i.v.). Increases in circulating concentrations of oxytocin, as determined by specific radioimmunoassay, confirmed that AV3V stimulation released oxytocin in both lactating and non-lactating rats. The increases in plasma oxytocin concentration evoked by electrical stimulation of the AV3V region were dependent upon intensity and frequency of stimulation, and electrode position. A significant (P less than 0.05) increase followed stimulation at 25 Hz and 0.1 mA, and a maximal response was obtained with 50 Hz and 1.0 mA. Stimulation of the area in and around the nucleus medianus produced the greatest rise in oxytocin secretion. The milk-ejection reflex was not abolished after acute electrolytic ablation of the AV3V region in urethane-anaesthetized lactating rats, but electrolytic lesion of the AV3V region prevented the increase in plasma oxytocin concentration which normally followed an osmotic stimulus (1 ml 1.5 mol NaCl/l, i.p.). These studies provide evidence that the AV3V region is a major source of excitatory afferents to oxytocin neurones; this input is essential for the osmoresponsiveness of these neurones but plays little role in the control of such neurones during reflex milk ejection.

Mammary resistance: a possible controlling factor in milk ejection

At 8 and 13 days post partum, rats have the same total milk availability; yet, in response to suckling they release a greater amount of milk on day 13 than on day 8. Increased sensitivity to suckling in the more advanced lactators may result from a greater release of oxytocin or from changes in the mammary glands as lactation advances. The present study explores this latter possibility in anaesthetized dams at 8-9 and 13-15 days of lactation. Milk release and intramammary pressure were measured in anaesthetized dams in response to various doses of oxytoxin. Milk release was determined from the body weight gain of pups which had been fasted for 5 h before suckling on dams which had been isolated for 5 h. This parameter was significantly greater in 13- to 15-day lactators than in 8- to 9-day lactators over the range of oxytocin doses examined. In contrast, intramammary peak pressure and its dissipation time were significantly larger in the 8- to 9-day lactators than in the 13- to 15-day lactators. The compliance of the mammary glands was indirectly assessed at the two stages of lactation. When a constant pressure pulse was introduced into a cannulated gland, the resulting pressure peak was significantly greater in 8-day than in 13-day lactators, indicating a greater resistance in the former. Taken together, these results indicate that when endogenous oxytocin is inhibited (by anaesthesia) the greater milk release observed at the later stage of lactation in response to various doses of oxytocin may be due to a decline in mammary resistance as lactation progresses.

Effects of porcine relaxin on oxytocin release from the neurohypophysis in the anaesthetized lactating rat.

The effect of relaxin on electrically evoked release of oxytocin from the posterior pituitary was examined by monitoring changes in intramammary pressure in the anaesthetized lactating rat. The amount of oxytocin released by electrical stimulation of the neurohypophysis in vivo was dramatically reduced following i.v. injection of highly purified porcine relaxin (2.5-10 micrograms/rat). Relaxin inhibited oxytocin release in a dose-dependent manner and the onset of inhibition occurred within 6-10 min and lasted for 10-60 min. No effect on the sensitivity of the mammary gland to exogenous oxytocin was observed after relaxin treatment. During the period of inhibition, i.v. injection of the opioid antagonist naloxone chloride (1 mg/kg) completely and immediately restored electrically evoked oxytocin release. The neurohypophysis is known to contain endogenous opioid peptides, therefore the effect of relaxin on electrically stimulated release of oxytocin from the rat isolated neural lobe in vitro was examined. Relaxin (500-2000 ng/ml) failed to inhibit oxytocin release in vitro. The results suggest that relaxin can inhibit the release of oxytocin from terminals in the neurohypophysis, but by an indirect mechanism. This action appears to be mediated through endogenous opioid peptides whose source is not clear. They are unlikely to be of neurohypophysial origin and may probably come from the adrenal medulla, since acute adrenalectomy negated the inhibitory effect of relaxin on oxytocin release.

Changing characteristics of the milk-ejection reflex during pregnancy, lactation and after weaning in the rat.

The pattern of reflex milk ejection during suckling was investigated in anaesthetized Wistar rats at various stages of pregnancy, lactation and after weaning. Milk-ejection responses were measured using intramammary pressure recordings, and the amount of oxytocin released was estimated from log dose-response lines compiled from the mammary responses to exogenous oxytocin. The number of rats showing intramammary pressure responses to oxytocin increased on Day 22 of pregnancy (the day of parturition) and decreased at 8 days after weaning. The dose-response lines from pregnant animals were shallow, but steepened and shifted to the left during lactation and after weaning. Reflex milk-ejection responses during suckling were detectable in primigravid animals, indicating that birth of the litter and previous suckling experience are unnecessary for the immediate functioning of the reflex. Reflex milk-ejection responses improved during early lactation (such that the frequency and the amount of oxytocin released at each response were maximal at Day 10 of lactation), and subsequently declined in late lactation. Although the frequency of responses in animals 2 and 4 days after weaning was similar to that in late lactating animals, the amount of oxytocin released at each response had risen again to mid-lactation values. In animals undergoing a second pregnancy and lactation the pattern of change in the milk-ejection responses was similar to that of primiparous animals.

Effets des prostaglandines PGF2α sur l'éjection du lait de la brebis. Conséquences de l'ovariectomie accompagnée ou non d'une complémentation œstroprogestative

The intrajugular administration of 200 micrograms of Dinolytic (tromethamine salt of PGF2 alpha) to lactating ewes caused an intramammary pressure (IMP) increase only during the luteal phase of the sexual cycle (group A). The increase in progesteronemia, induced by three daily injections of 2.5 micrograms of LH-RH, did not modify response amplitude (group B). On the other hand, bilateral ovariectomy (groupe C) led to the suppression of those responses, but supplementary oestroprogestative (table 1) did not re-establish them. It is probable that the milk ejection caused by PGF2 alpha resulted from a release of oxytocin by the corpus luteum. The ineffectiveness of the exogenous and endogenous reinforcement of progesterone therefore suggests that this hormone plays no part in the putative control of hypothalamic receptivity to prostaglandins.