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8. Nursing Intervention and Summary of Evidence Pertaining to Neonatal Recurrent Hypoglycemia Induced by Terbutaline

Author

Wang,Meng-qin, Zhuang,Ying, Zheng,Ya-ning, Wang,Meng-qin, Zhuang,Ying, and Zheng,Ya-ning

Abstract

Meng-qin Wang,1,* Ying Zhuang,1,* Ya-ning Zheng2 1Department of Obstetrics, Nanjing Drum Tower Hospital, Nanjing, People’s Republic of China; 2Department of Gynecology Otolaryngology, Nanjing Drum Tower Hospital, Nanjing, People’s Republic of China*These authors contributed equally to this workCorrespondence: Ya-ning Zheng, Email zhengyaqinzyq@126.comBackground: Neonatal hypoglycemia (NH) is a common clinical symptom that can occur in both normal and critically ill neonates. The placenta is the site of material exchange between the mother and the fetus, a special organ shared by the mother and the fetus during pregnancy, and one of its important functions is to transfer nutrients from the mother to the fetus. Terbutaline is used to relax frequent uterine contractions before delivery, and it can penetrate the placental barrier and affect the normal decomposition of neonatal glycogen. The situation is neonatal hypoglycemia if not timely detection and interventions in time, the neonate may have recurrent hypoglycemia, leading to irreversible nervous system damage, such as neonatal hypoglycemic encephalopathy, and visual and cognitive impairment.Case Report: The male neonate was a single fetus, with a birth weight of 3660 g and a length of 50 cm. The blood glucose at birth was 5 mmol/L, Apgar score was 9– 10, and body temperature was normal. The mother was healthy, was not diabetic, and had no other risk factors for neonatal hypoglycemia. She was injected with 0.25 mg of terbutaline 6 hours before delivery due to frequent uterine contractions. However, it was found that recurrent hypoglycemia occurred in the neonate even after adequate oral feeding.Conclusion: We included evidence-based use of terbutaline 48 hours before delivery as a high-risk factor for hypoglycemia in the rooming-in neonatal hypoglycemia care program, and formulate the corresponding nursing process, with good effect.Keywords: hypoglycemia, neonatal recurrent hypoglycemia

Published
2023

12. [Effect of methyl eugenol on hypoxia/reoxygenation injury of human renal tubular epithelial cells and its mechanism].

Author

Kuang BC, Hou SH, Zhan GJ, Wang MQ, Zhang JS, Sun KL, Wang ZH, Li QW, and Gong NQ

Subjects
Apoptosis, Epithelial Cells metabolism, Heme Oxygenase-1 metabolism, Humans, Hypoxia, NF-E2-Related Factor 2 genetics, NF-E2-Related Factor 2 metabolism, Oxidative Stress, Reactive Oxygen Species, Eugenol analogs & derivatives, Eugenol pharmacology, Reperfusion Injury drug therapy
Abstract

This study aimed to investigate the effect of methyl eugenol(ME) on hypoxia/reoxygenation(H/R)-induced injury of human renal tubular epithelial HK-2 cells and its mechanism. The viability of HK-2 cells cultured with different concentrations of ME and exposed to H/R was detected by cell counting kit-8(CCK-8) assay. The effect of ME on the morphology of HK-2 cells was observed under an inverted microscope. The content of intracellular reactive oxygen species in different groups was detected after 2',7'-dichlorodihydrofluorescein diacetate(DCFH-DA) fluorescence staining. Cell apoptosis was determined by flow cytometry. Changes in mitochondrial membrane potential were monitored by JC-1 dye. The concentrations of nuclear factor erythroid 2 related factor 2(Nrf2), heme oxygenase-1(HO-1), and nicotinamide adenine dinucleotide phosphatase oxidase 4(Nox4) were measured by Western blot, followed by the assay of Nrf2 concentration changes in cytoplasm and nucleus by confocal fluorescence staining. The results showed that when the concentration of ME was 0-40 μmol·L~(-1), the activity of HK-2 cells was not affected. Compared with the model group, ME enhanced the activity of HK-2 cells and the cell morphology was normal. As revealed by further experiments, ME inhibited the release of reactive oxygen species and the decline in mitochondrial membrane potential of HK-2 cells after H/R injury, promoted Nrf2/HO-1 expression and Nrf2 translocation to the nucleus, and down-regulated the expression of Nox4, thereby significantly reducing apoptosis. This protective effect of ME could be reversed by the specific Nrf2 inhibitor ML385. These findings have preliminarily proved that ME effectively protected HK-2 cells against H/R injury, which might be related to its promotion of Nrf2/HO-1 signaling pathway and inhibition of Nox4. Such exploration on the possible mechanism of ME in the treatment of renal ischemia-reperfusion injury(IRI) and protection of organ function from the perspective of antioxidant stress has provided reference for related research on the treatment of acute kidney injury with traditional Chinese medicine.

Published
2021
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