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Suction pressure has been reported to be a key driving force of lactation. An infant's sucking at its mother's breasts is the major stimulus to post-natal prolactin (PRL) secretion, and PRL is the essential hormone for lactation and milk production. It is unknown what role suction pressure has in PRL secretion and milk supply postnatally.To explore the relationship between the suction pressure, PRL level, lactation, and milk supply in breastfeeding mother-infant dyads.Healthy women with normal full-term infants were enrolled (n = 122). Data collection included suction pressure, PRL level, and the mother's perception of both the onset of her lactation and her milk supply at 1 month. Suction pressure was measured with a pressure sensor connected to a tube placed alongside the nipple. The chemiluminescence method was used to quantify maternal serum PRL level both before and after a breastfeed to explore the effect of suckling on PRL increment. The mother's perception of the onset of her lactation was evaluated by the mother's sense of fullness in her breast. The mother's perception of milk supply was evaluated by using the HH Lactation Scale.Data from 117 participants were included in this analysis. Low suction pressure, a shorter gestational age, a high pre-gestational body mass index (BMI), and high infant birth weight were associated with a smaller than average PRL increment. High suction pressure, longer sucking duration, and a low gestational weight gain were related to a mother's perception of an earlier onset of her lactation. However, low suction pressure, a high frequency of giving formula, a small PRL increment, and the mother's perception of a later onset of her lactation were correlated with her perception of an insufficient milk supply.Suction pressure varied directly with the post-natal PRL increment. Suction pressure was associated with the timing of the mother's perception of her lactation. Strong suction pressure by the infant is likely to enhance the mother's confidence in her lactation. Additionally, sucking duration, frequency of giving formula, maternal BMI, and infant birth weight played a role in early breastfeeding success.

Objectives:To explore whether newborns born via Cesarean section have a weaker intraoral vacuum compared with those born vaginally and to determine whether a weaker intraoral vacuum is related to a delayed onset of lactation.Methods:For this prospective cohort study, 71 mother–infant dyads were enrolled and divided into birthing groups, vaginal or Cesarean. The newborn intraoral vacuum was measured via a tube placed alongside the nipple and connected to a pressure sensor during a breast-feeding session within the first 24 hr after birth. Onset of lactation was confirmed by maternal perception of breast fullness. The intraoral vacuum and its relationship with the onset of lactation were analyzed. Results: After adjustment for confounding factors, the peak intraoral vacuum was −19.50 kPa in the vaginal group, which was significantly stronger than the −13.78 kPa in the Cesarean group ( p = .005). Additionally, the baseline intraoral vacuum in the vaginal group (−2.35 kPa) was significantly stronger than that in the Cesarean group (−1.18 kPa; p = .022). Strength of the newborn intraoral vacuum was associated with the time of onset of maternal lactation.Conclusion:Cesarean section may weaken newborns’ intraoral vacuum within the first 24 hr after birth. Stronger intraoral vacuum was related to earlier onset of lactation. Early intervention aimed at the weaker intraoral vacuum should be provided to promote the onset of lactation.

Mechanical enemas can lead to intestinal mucosal injuries and bowel barrier damage, presenting as electrolyte disturbances and functional intestinal disorders. Most researchers believe that the mechanism of injury is related to osmolality, volume and temperature of the solution, infusion pressure, and the composition of the enema tube. We hypothesized that the pH of the enema solution may also contribute to intestinal damage. We administered enema solutions—normal saline, soapsuds, or vinegar (neutral, alkaline, or acidic solutions, respectively)—to three groups of rabbits ( n = 20 per group). The solutions were standardized for volume and temperature and the soapsuds and vinegar solutions were adjusted to be isotonic with normal saline or deionized water. We also included a control group ( n = 20) in which the enema tubes were inserted but no solution was administered. We biopsied 3 sites (rectum and distal and proximal colon). Damage to intestinal mucosa was observed by light microscopy and transmission electron microscopy. In order to explore the detection of damage using noninvasive methods, cyclooxygenase (COX)-2 gene expression was measured in the exfoliated cells gathered from postenema defecation. Epithelial loss, inflammatory reaction, and cellular microstructure damage was increased in the vinegar and soapsuds groups. Also, exfoliated cells in these groups had higher COX-2 expression than the normal saline group. The acidic and alkaline enema solutions thus caused more severe damage to the intestinal mucosa compared to the neutral liquid, supporting our hypothesis. Further, the detection of COX-2 expression shows promise as a noninvasive method for estimating enema-induced damage.

Background The purpose of this study was to determine the functional relationship between tidal volume (V T ) and 4 other ventilator parameters. Methods The following parameters were collected from an AVEA ventilator operating in the volume-controlled ventilation mode: V T (in L), peak flow (V max , in L/min), breath rate (f, in bpm), inspiratory-to-expiratory time ratio (I:E) and plateau time (T P , in s). The relationship between V T and each of the other variables was determined. Results When the other parameters were held constant, V T was positively correlated with V max and I:E, but negatively correlated with f and T P . When the velocity versus time curve was a 50% linearly decreasing wave, the functional relationship among the 5 parameters was governed by the equation: V T = 180 V max (60f – 60f [1 + I:E] – T P ). Conclusions The functional relationship among the 5 parameters for the AVEA ventilator in the volume-controlled ventilation mode was determined. The parameters should be controlled in accordance with the patient’s pathophysiological needs.