MAMMARY OXYGEN TENSION AND THE MILK-EJECTION MECHANISM

1962 ◽  
Vol 23 (4) ◽  
pp. 375-384 ◽  
Author(s):  
B. A. CROSS ◽  
I. A. SILVER

SUMMARY 1. Polarographic recording of pO2 from gold-plated needle electrodes inserted into lactating mammary glands of rabbits under light urethane anaesthesia gave resting values of 15–30 mm. Hg. Expelling the milk from distended glands raised the pO2 level. 2. Myoepithelial contraction (milk ejection) induced by i.v. injection of oxytocin lowered pO2 by an amount depending on the rise in intramammary pressure. 3. Surgical shock, spinal anaesthesia or i.v. injection of adrenaline depressed mammary pO2 and reduced the milk-ejection response to i.v. oxytocin. 4. When mammary pO2 was raised by O2 breathing, or lowered by N2 breathing, the milk-ejection response to i.v. oxytocin was not affected. 5. Electrical stimulation of the lateral and posterior hypothalamic areas reduced mammary pO2 and milk ejection in a way similar to i.v. adrenaline. Bilateral electrolytic lesions in these areas produced a sustained depression of mammary pO2. 6. It is concluded that the pO2 of mammary tissues gives a measure of capillary blood flow and that this, rather than the absolute pO2 level, determines the response of the myoepithelium to circulating oxytocin.

1953 ◽  
Vol 9 (1) ◽  
pp. 7-18 ◽  
Author(s):  
B. A. CROSS

1. Emotional inhibition of the milk-ejection reflex in rabbits is described. 2. Injection of 5–50 μg adrenaline intravenously into does before nursing interfered with milk ejection, as shown by the failure of the young to withdraw more than three-quarters of the normal yield of milk. Injection of 150 mU (=milliunits) 'Pitocin' immediately after the adrenaline did not restore normal milk ejection. 3. Intravenous injection of 5 μg adrenaline suppressed the milk-ejection response to 50 mU posterior pituitary extract in anaesthetized rabbits with cannulated teats, provided the injection of adrenaline preceded that of the posterior pituitary extract. The inhibitory effect had not entirely disappeared in 2 min. 50μg adrenaline prevented the occurrence of milk ejection for 3½ min. 4. Intravenous doses of 5 μg adrenaline, but not smaller amounts, inhibited the milk-ejection response to electrical stimulation of the supraoptico-hypophysial tract, if injected before stimulation or during the latent period of the response. When injected after the commencement of milk ejection 5 μg adrenaline was without effect, but 50 μg abolished the response. 5. Electrical stimulation of the posterior hypothalamus produced inhibition of the milk-ejection response to injected oxytocic extract, together with pupillary dilatation and exophthalmos. The inhibition closely resembled that resulting from injection of adrenaline. 6. It is concluded that one mechanism involved in the emotional inhibition of milk ejection is an activation of the sympathetico-adrenal system, resulting in antagonism of the action of the neurohypophysial milk-ejection hormone on the contraction process within the mammary gland.


1993 ◽  
Vol 113 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Tian-Ying Ren ◽  
E. Laurikainen ◽  
W. S. Quirk ◽  
J. M. Miller ◽  
A. L. Nuttall

1988 ◽  
Vol 118 (3) ◽  
pp. 471-483 ◽  
Author(s):  
L. M. Voloschin ◽  
E. Décima ◽  
J. H. Tramezzani

ABSTRACT Electrical stimulation of the XIII thoracic nerve (the 'mammary nerve') causes milk ejection and the release of prolactin and other hormones. We have analysed the route of the suckling stimulus at the level of different subgroups of fibres of the teat branch of the XIII thoracic nerve (TBTN), which innervates the nipple and surrounding skin, and assessed the micromorphology of the TBTN in relation to lactation. There were 844 ± 63 and 868 ± 141 (s.e.m.) nerve fibres in the TBTN (85% non-myelinated) in virgin and lactating rats respectively. Non-myelinated fibres were enlarged in lactating rats; the modal value being 0·3–0·4 μm2 for virgin and 0·4–0·5 μm2 for lactating rats (P > 0·001; Kolmogorov–Smirnov test). The modal value for myelinated fibres was 3–6 μm2 in both groups. The compound action potential of the TBTN in response to electrical stimulation showed two early volleys produced by the Aα- and Aδ-subgroups of myelinated fibres (conduction velocity rate of 60 and 14 m/s respectively), and a late third volley originated in non-myelinated fibres ('C') group; conduction velocity rate 1·4 m/s). Before milk ejection the suckling pups caused 'double bursts' of fibre activity in the Aδ fibres of the TBTN. Each 'double burst' consisted of low amplitude action potentials and comprised two multiple discharges (33–37 ms each) separated by a silent period of around 35 ms. The 'double bursts' occurred at a frequency of 3–4/s, were triggered by the stimulation of the nipple and were related to fast cheek movements visible only by watching the pups closely. In contrast, the Aα fibres of the TBTN showed brief bursts of high amplitude potentials before milk ejection. These were triggered by the stimulation of cutaneous receptors during gross slow sucking motions of the pup (jaw movements). Immediately before the triggering of milk ejection the mother was always asleep and a low nerve activity was recorded in the TBTN at this time. When reflex milk ejection occurred, the mother woke and a brisk increase in nerve activity was detected; this decreased when milk ejection was accomplished. In conscious rats the double-burst type of discharges in Aδ fibres was not observed, possibly because this activity cannot be detected by the recording methods currently employed in conscious animals. During milk ejection, action potentials of high amplitude were conveyed in the Aα fibres of the TBTN. During the treading time of the stretch reaction (SR), a brisk increase in activity occurred in larger fibres; during the stretching periods of the SR a burst-type discharge was again observed in slow-conducting afferents; when the pups changed nipple an abrupt increase in activity occurred in larger fibres. In summary, the non-myelinated fibres of the TBTN are increased in diameter during lactation, and the pattern of suckling-evoked nerve activity in myelinated fibres showed that (a) the double burst of Aδ fibres, produced by individual sucks before milk ejection, could be one of the conditions required for the triggering of the reflex, and (b) the nerve activity displayed during milk-ejection action may result, at least in part, from 'non-specific' stimulation of cutaneous receptors. J. Endocr. (1988) 118, 471–483


1997 ◽  
Vol 17 (6) ◽  
pp. 686-694 ◽  
Author(s):  
Elvire Vaucher ◽  
Josiane Borredon ◽  
Gilles Bonvento ◽  
Jacques Seylaz ◽  
Pierre Lacombe

We earlier reported that electrical stimulation of the rat nucleus basalis of Meynert (NBM) induces large cerebral blood flow increases, particularly in frontal cortical areas but also in some subcortical regions. The present study was designed to address the issue of blood flow control exerted by NBM projections. To this aim, we have determined whether these flow increases were associated with proportionate changes in metabolic activity as evaluated by cerebral glucose utilization (CGU) strictly under the same experimental conditions in the conscious rat. An electrode was chronically implanted in a reactive site of the NBM as determined by laser-Doppler flowmetry (LDF) of the cortical circulation. One to two weeks later, while the cortical blood flow was monitored by LDF, we measured CGU using the [14C]2-deoxyglucose autoradiographic technique during unilateral electrical stimulation of the NBM, and analyzed the local flow-metabolism relationship. The large increases in cortical blood flow induced by NBM stimulation, exceeding 300% in various frontal areas, were associated with at most 24% increases in CGU (as compared with the control group) in one frontal area. By contrast, strong increases in CGU exceeding 150% were observed in subcortical regions ipsilateral to the stimulation, especially in extrapyramidal structures, associated with proportionate CBF changes. Thus, none of the blood flow changes observed in the cortex can be ascribed to an increased metabolic activity, whereas CBF and CGU were coupled in many subcortical areas. This result indicates that different mechanisms, which do not necessarily involve any metabolic factor, contribute to the regulation of the cerebral circulation at the cortical and subcortical level. Because the distribution of the uncoupling is coincident with that of cholinergic NBM projections directly reaching cortical microvessels, these data strongly support the hypothesis that NBM neurons are capable of exerting a neurogenic control of the cortical microcirculation.


2020 ◽  
Vol 46 (4) ◽  
pp. 384-390
Author(s):  
G. I. Lobov ◽  
Yu. P. Gerasimenko ◽  
T. R. Moshonkina

1993 ◽  
Vol 265 (4) ◽  
pp. R733-R738 ◽  
Author(s):  
H. Izumi ◽  
K. Karita

Local application of capsaicin (threshold dose 150 microM) or nicotine (threshold dose 15 mM) to the nasal mucosa as well as electrical stimulation (threshold intensity 10 V) of the nasal mucosa elicited dose- or intensity-dependent blood flow increases in the ipsilateral lower lips of the anesthetized cats. Pretreatment with 3 mM capsaicin applied locally to the nasal mucosa abolished or reduced the vasodilation in response to capsaicin, nicotine, and ammonia vapor but not to light mechanical or electrical stimulation of the nasal mucosa. The blood flow increases elicited by all above stimuli were greatly reduced by pretreatment with hexamethonium, an autonomic ganglion blocker. These results suggest that stimulation of the nasal mucosa by chemical (capsaicin, nicotine, ammonia), mechanical, or electrical methods elicits the autonomic reflex vasodilatation in the cat lower lips. Furthermore, there seem to be at least two types of afferent fibers in the nasal mucosa of the cats: one type is capsaicin-sensitive fibers, while another type is capsaicin-resistant fibers involved in reflex vasodilatation.


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