Introduction: Women's sexual health is a vital and important part of life at any age. In particular, pregnancy and childbirth bring biological, psychological, and social changes which may influence sexual health. It has been shown that sexual function declines during pregnancy and does not return to its baseline levels during the postpartum period. Despite the complexity and significance of this subject, health providers often neglect sexual aspects during pregnancy and postpartum. Aim: We believe that clarifying the risk factors will help open conversations and improvements in sexual function. Methods: In this review, we focus on how postpartum sexual function is affected by mode of delivery, perineal trauma during delivery, episiotomy, and lactation. Concclusions: We conclude that the mode of delivery has no significant effect on short-and long-term postpartum sexual function. On the other hand, 3rd and 4th degree tears are strongly associated with postpartum sexual dysfunction. We found that episiotomy does not adversely affect sexual function, and lactation has a slightly negative effect. We believe that shedding light on this topic will lead to a better understanding for pregnant and postpartum women and the obstetrician. Further studies may elucidate more useful treatment approaches.
Introduction
Preterm infants with necrotizing enterocolitis (NEC) are at increased risk of cerebral injury and neurodevelopmental dysfunction. N‐acetyl‐cysteine (NAC) is a known anti‐inflammatory and antioxidant agent. Currently, there is no prophylactic treatment in clinical use to prevent NEC and its neurodevelopmental sequelae. We sought to determine whether brain inflammation/apoptosis accompanies NEC systemic inflammation, and whether it can be attenuated by maternal NAC treatment during pregnancy and/or in the neonatal period in a rat model.
Material and methods
An established NEC newborn model (hypoxia 5% O2 for 10 min and formula feeding thrice daily, beginning on day 1 for 4 days) was used in Sprague‐Dawley rat pups (n = 32). An additional group of pups (n = 33) received NAC (300 mg/kg intraperitoneal thrice daily) in addition to NEC conditions (NEC‐NAC). Control pups (n = 33) were nursed and remained with the dam in room air. Two additional groups included pups of dams treated once daily with NAC (300 mg/kg intravenous) in the last 3 days of pregnancy. After birth, pups were randomized into NAC‐NEC (n = 33) with NEC conditions and NAC‐NEC‐NAC (n = 36) with additional postnatal NAC treatment. Pups were sacrificed on the fifth day of life. Pup serum interleukin (IL)‐6 protein levels, and brain nuclear factor kappa B (NF‐κB) p65, neuronal nitric oxide synthase (nNOS), Caspase 3, tumor necrosis factor alpha (TNF‐α), IL‐6 and IL‐1β protein levels were determined by ELISA, western blot and TUNEL staining, and the groups were compared using analysis of variance (ANOVA).
Results
NEC pups had significantly increased serum IL‐6 levels compared with the control group as well as increased neuronal apoptosis and brain protein levels of NF‐κB, nNOS, Caspase 3, TNF‐α, IL‐6 and IL‐1β compared with control. In all NAC treatment groups, levels of serum IL‐6, neuronal apoptosis and brain NF‐κB, nNOS, Caspase 3, TNF‐α, IL‐6 and IL‐1β protein levels were significantly reduced compared with the NEC group. The most pronounced decrease was demonstrated within the NAC‐NEC‐NAC group.
Conclusions
NAC treatment can attenuate newborn inflammatory response syndrome and decrease offspring brain neuroapoptosis and inflammation in a rat model of NEC by inhibition of NF‐κB, nNOS and Caspase 3 pathways.
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