Natural latex-glycerol dressing to reduce nipple pain and healing the skin in breastfeeding women.

BACKGROUND: Nipple pain is the second most common reason for early weaning, exceeded only by the insufficient milk supply. Nipple fissures can bring other problems, acting also as a portal for bacteria and leading to mastitis. This work proposes the breast protector composite development using materials with tissue repair and moisturizing properties, aligned with a low-cost procedure, aiming not only to relieve pain, but also to heal the nipple fissures caused by breastfeeding. MATERIALS AND METHODS: For the dressings, production was used Natural Latex extracted from the rubber tree and glycerol. The Samples were evaluated chemically and physically by the techniques of Scanning Electron Microscopy, Fourier transform infrared spectroscopy, mechanical traction, and contact angle. The samples were also biologically evaluated by the hemolytic and cytotoxic activity assays. RESULTS: From the physical-chemical assays, the matrix with glycerol has high pore density; the natural latex and glycerol do not covalently interact, indicating that the glycerol can be released; the glycerol addition makes the matrix more elastic but fragile, and increase the wettability. From the biological assays, both materials showed no hemolytic effects; and the cytotoxicity results showed that glycerol did not present cytotoxicity in the fibroblasts, but show a dose-dependent influence in the keratinocytes. CONCLUSION: The material developed for application in breast fissures has mechanical properties similar to those found for materials for dermal applications, present high wettability and pore density. Furthermore, the material showed no cytolytic activity and the tests with skin cell cultures demonstrated the biocompatibility.

Sympathetic innervation of mammary glands mediates suckling-induced reflex inhibition of milk yield in rats.

Previous work has shown that physiologic activation of the sympathetic system may inhibit milk yield (ME) in rats. Thus, adrenal catecholamines (CAs) are released by suckling, but it is not known whether such inhibition results also from reflex activation by the same stimulus of neural sympathetics upon the mammary gland. The present experiments were designed to determine whether suckling inhibits ME induced by oxytocin (OT) in the urethane-anesthetized lactating rat, and whether such inhibition results from adrenal and/or neurally released CAs. Rats were isolated (6 h) from their pups and then anesthetized. OT (0.8 mU every 2 min) was administered intravenously to the mothers during suckling. Rats were either chronically implanted with cannulae into the lateral cerebral ventricles (intracerebroventricularly), bilaterally adrenalectomized (ADX), hypophysectomized (HX), spinal cord transected (SCT: T3-T4), or had the nipple area (NA) locally anesthetized before suckling. MEs were low in control, sham, ADX and HX rats, but not in rats given the beta-adrenergic blocker propranolol (PROP; intravenously or intracerebroventricularly injected), nor in SCT, NA or PROP-HX rats. As revealed by ductal resistance measurements as an indicator of ductal tone, suckling-induced inhibition of ME was due to ductal constriction within the mammary glands. These effects of suckling, however, could be prevented by prior activation of ductal mechanoreceptors. Together, these results indicate that suckling inhibits ME through the reflex activation of neurally mediated central beta-adrenergic mechanisms, and that these effects, in turn, can be regulated by ductal mechanoreceptor activation.

Prolactin stimulates emission of nipple pheromone in ovariectomized New Zealand white rabbits.

Using ovariectomized New Zealand white rabbits and the nipple-search behavior of pups as a bioassay, we evaluated the capacity of prolactin to stimulate the emission of an odor signal that allows newborn pups to locate the mother's nipples and suckle. Whereas emission of this so-called nipple pheromone was minimal in untreated, ovariectomized does, emission was stimulated by the administration of progesterone (1 mg/day) to estrogen-treated does (0.5 microgram estradiol benzoate/day) and decreased after withdrawal of progesterone despite continuous administration of estrogen. However, substituting ovine prolactin (1.5 mg/day) for progesterone, under continuous estrogen administration, resulted in an increase in pheromone emission to near-maximal levels. This stimulatory effect of prolactin was not progesterone-dependent since it also occurred in does pretreated with estrogen alone and, to a lesser extent, even in females without estrogen priming. From these and previous data, we propose that emission of nipple pheromone in the rabbit is induced during pregnancy by the combined action of estrogen and progesterone, and maintained during lactation by the dual action of estrogen and prolactin.