The Role of Magnesium Sulfate in the Treatment of Persistent Pulmonary Hypertension in the Neonate : Our Experience in King Hussein Medical Centre (KHMC)

2020 ◽  
Vol 27 (2) ◽  
pp. 21-26
Author(s):  
Ayash , Fadi Farhan ◽  
Saleh , Alaeddin Ali ◽  
Alyassen , Abdalrazzaq Ahmad ◽  
Alhadidi , Aghadir Mohammad
1995 ◽  
Vol 10 (6) ◽  
pp. 270-282
Author(s):  
Stella Kourembanas

Persistent pulmonary hypertension of the newborn (PPHN) is a common cause of respiratory failure in the full-term neonate. Molecular and cellular studies in vascular biology have revealed that endothelial-derived mediators play a critical role in the pathogenesis and treatment of PPHN. Endothelial-derived vasoconstrictors, like endothelin, may increase smooth muscle cell contractility and growth, leading to the physiologic and structural changes observed in the pulmonary arterioles of infants with this disease. On the other hand, decreased production of the endothelial-derived relaxing factor, nitric oxide, may exacerbate pulmonary vasoreactivity and lead to more severe pulmonary hypertension. Exogenous (inhaled) nitric oxide therapy reduces pulmonary vascular resistance and improves oxygenation. The safety and efficacy of this therapy in reducing the need for extracorporeal membrane oxygenation and decreasing long-term morbidity is being tested in several trials nationally and abroad. Understanding the basic mechanisms that regulate the gene expression and production of these vasoactive mediators will lead to improved preventive and therapeutic strategies for PPHN.


2021 ◽  
Vol 20 (10) ◽  
pp. 2163-2169
Author(s):  
Shuping Huang ◽  
Tao Zhong

Purpose: To investigate the efficacy of the combined use of sildenafil and magnesium sulfate in the treatment of persistent pulmonary hypertension of the newborn (PPHN), and its influence on hemodynamics.Methods: A total of 174 children with persistent pulmonary hypertension who were treated in Ganzhou People’s Hospital, Ganzhou, China were selected and randomly assigned to joint group (JG) and control group (CG), with 87 patients in each group. The CG group received magnesium sulfate, while the JG group received sildenafil plus magnesium sulphate. The respiratory parameters of the children were analyzed using blood gas analyzer, while their hemodynamic indices were evaluated using color Doppler echocardiography. The levels of cytokines and inflammatory factors were determined by enzyme-linked immunosorbent assay (ELISA).Results: Time taken for symptom disappearance, oxygen therapy, and hospitalization period were shorter in JG than in CG (p < 0.05). Post-treatment, the respiratory parameters (PaO2, PaCO2, and SaO2) in both groups s improved, with lower levels of PaO2 and PaCO2, and a higher level of SaO2 in JG (p < 0.05). Following treatment, the levels of systemic vascular resistance (SVR), posterior pulmonary vascular resistance (PVR) and pulmonary artery pressure (PA) in JG were significantly reduced, relative to CG (p < 0.05). Similarly, the expression of endothelin -1 (ET-1), brain natriureticpeptide (BNP), and angiotensin 1 (ANG-1) improved, with lower levels of ET-1 and BNP, and a higher level of ANG-1 in JG (p < 0.05). There was post-treatment reduction as well in IL-6 and TNF-α, with lower levels in JG (p < 0.05). Patients in JG showed higher total treatment effectiveness and a lowerincidence of adverse reactions than those in CG (p < 0.05).Conclusion: The combined use of sildenafil and magnesium sulfate enhances the management of PPHN, ameliorates respiratory parameters, hemodynamics, and levels of cytokines and inflammatory factors. These findings provide evidence-based medical references for a new treatment strategy for PPHN.


2015 ◽  
Vol 93 (3) ◽  
pp. 185-194 ◽  
Author(s):  
Jena Fediuk ◽  
Shyamala Dakshinamurti

Persistent pulmonary hypertension of the newborn (PPHN) is defined as the failure of normal pulmonary vascular relaxation at birth. Hypoxia is known to impede postnatal disassembly of the actin cytoskeleton in pulmonary arterial myocytes, resulting in elevation of smooth muscle α-actin and γ-actin content in elastic and resistance pulmonary arteries in PPHN compared with age-matched controls. This review examines the original histological characterization of PPHN with attention to cytoskeletal structural remodeling and actin isoform abundance, reviews the existing evidence for understanding the biophysical and biochemical forces at play during neonatal circulatory transition, and specifically addresses the role of the cortical actin architecture, primarily identified as γ-actin, in the transduction of mechanical force in the hypoxic PPHN pulmonary circuit.


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