RESUMO
Objective: This study aimed to investigate the relationship between the thickness of the uterine muscle layer at placenta attachment and postpartum hemorrhage, and to evaluate the predictive value of this thickness in identifying high-risk patients. It provides a theoretical basis for early identification and screening of pregnant women at high risk of postpartum hemorrhage, and reduces the occurrence of serious complications of postpartum hemorrhage. Method: A total of 378 pregnant women admitted to the Second People's Hospital of Shantou City from January to December 2021 were enrolled in this study. High-risk patients were defined as those with a uterine muscle layer thickness at placenta attachment greater than 2.5 cm, as measured by transabdominal ultrasound. Postpartum blood loss and hemoglobin changes were measured before and after delivery. Stratified analysis was conducted based on various patient characteristics, and the predictive value of the thickness was determined using ROC curve analysis. By providing the specific criteria for defining high-risk patients, readers can better understand the methodology used in this study. Results: The linear regression analysis showed a significant negative correlation between the thickness of the uterine muscle layer at placenta attachment and postpartum blood loss at 2 hours (t value = -6.9848, P = 1.33E-11 < .05). There was also a significant negative correlation between the thickness and hemoglobin changes before and after delivery (t value = -2.242, P = .026 < .05). These findings indicate a robust association between uterine muscle layer thickness and both postpartum blood loss and hemoglobin changes. ROC curve analysis revealed that the thickness of the uterine muscle layer at placenta attachment had predictive value for postpartum hemorrhage. This suggests that measuring the thickness of the uterine muscle layer can serve as a reliable predictor for identifying women at risk of postpartum hemorrhage. Additionally, stratified analysis showed that the thickness had significant predictive value in certain subgroups of patients. Conclusion: The findings of this study demonstrate that the thickness of the uterine muscle layer at placenta attachment is a critical indicator for predicting postpartum hemorrhage. Specifically, the study shows a robust negative correlation between uterine muscle layer thickness and postpartum blood loss, as well as significant predictive value for identifying high-risk patients for postpartum hemorrhage. These results have important practical implications for clinical practice. With early identification of high-risk groups based on uterine muscle layer thickness measurements, clinicians can implement interventions to reduce the incidence and severity of postpartum hemorrhage, which may lead to improved patient outcomes and reduced healthcare costs. Overall, this study provides a theoretical basis for the development of targeted prevention strategies and risk management protocols, which may help reduce serious complications of postpartum hemorrhage and improve maternal and neonatal health.
RESUMO
The renal phenotype of EAST syndrome, a disease caused by the loss-of-function-mutations of Kcnj10 (Kir4.1), is a reminiscence of Gitelman's syndrome characterized by the defective function in the distal convoluted tubule (DCT). The aim of the present study is to test whether antidiuretic hormone (vasopressin)-induced stimulation of the Na(+)-activated 80-150pS K(+) channel is responsible for compensating the lost function of Kcnj10 in the thick ascending limb (TAL) of subjects with EAST syndrome. Immunostaining and western blot showed that the expression of aquaporin 2 (AQP2) was significantly higher in Kcnj10(-/-) mice than those of WT littermates, suggesting that the disruption of Kcnj10 stimulates vasopressin response in the kidney. The role of vasopressin in stimulating the basolateral K(+) conductance of the TAL was strongly indicated by the finding that the application of arginine-vasopressin (AVP) hyperpolarized the membrane in the TAL of Kcnj10(-/-) mice. Application of AVP significantly stimulated the 80-150pS K(+) channel in the TAL and this effect was blocked by tolvaptan (V2 receptor antagonist) or by inhibiting PKA. Moreover, the water restriction for 24h significantly increased the probability of finding the 80-150pS K(+) channel and the K(+) channel open probability in the TAL. The application of a membrane permeable cAMP analog also mimicked the effect of AVP and activated this K(+) channel, suggesting that cAMP-PKA pathway stimulates the 80-150pS K(+) channels. The role of the basolateral K(+) conductance in maintaining transcellular Cl(-) transport is further suggested by the finding that the inhibition of basolateral K(+) channels significantly diminished the AVP-induced stimulation of the basolateral 10pS Cl(-) channels. We conclude that vasopressin stimulates the 80-150pS K(+) channel in the TAL via a cAMP-dependent mechanism. The vasopressin-induced stimulation of K(+) channels is responsible for compensating lost function of Kcnj10 thereby rescuing the basolateral K(+) conductance which is essential for the transport function in the TAL.