Research and Reports in Pulmonology

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Commentary - Research and Reports in Pulmonology (2023) Volume 4, Issue 2

Novel Therapeutic Approaches for Neurogenic Pulmonary Edema: Targeting Endothelial Dysfunction and Oxidative Stress.

Natsuo Ogawa*

Department of Respiratory Medicine and Infectious Diseases, Oita University of Medicine, Oita, Japan

Corresponding Author:
Natsuo Ogawa
Department of Respiratory Medicine and Infectious Diseases
Oita University of Medicine, Oita, Japan
E-mail: ogawa.nat@lia.jp

Received: 05-Mar-2023, Manuscript No. AARRP-23-91249; Editor assigned: 07-Mar-2023, PreQC No. AARRP-23-91249(PQ); Reviewed: 21-Mar-2023, QC No. AARRP-23-91249; Revised: 25-Mar-2023, Manuscript No. AARRP-23-91249(R); Published: 01-Apr-2023, DOI:10.35841/aarrp-4.2.136

Citation: Ogawa N. Novel therapeutic approaches for neurogenic pulmonary edema: Targeting endothelial dysfunction and oxidative stress. Res Rep Pulmonol. 2023;4(2):136

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Abstract

Neurogenic pulmonary edema (NPE) is a serious complication that occurs in patients with various central nervous system (CNS) disorders. It is characterized by the accumulation of fluid in the lungs due to increased permeability of the pulmonary capillaries. NPE is a life-threatening condition that requires urgent medical attention. The current treatment options for NPE are limited, and there is a need for novel therapeutic approaches. In this commentary, we discuss the potential of targeting endothelial dysfunction and oxidative stress as new therapeutic strategies for NPE.

Keywords

Neurogenic pulmonary edema, Endothelial dysfunction, Oxidative stress, Central nervous system.

Introduction

Neurogenic Pulmonary Edema (NPE) is a complication that occurs in patients with various CNS disorders, such as traumatic brain injury, subarachnoid haemorrhage, and seizures. The underlying mechanisms of NPE are complex and involve changes in the sympathetic nervous system, inflammation, and increased permeability of the pulmonary capillaries [1]. The accumulation of fluid in the lungs can lead to respiratory failure and death if not treated promptly. The current treatment options for NPE are limited, and there is a need for new therapeutic approaches.

Endothelial dysfunction and oxidative stress are two potential targets for the development of novel therapeutic approaches for NPE [2]. Endothelial dysfunction is characterized by a reduction in the production of nitric oxide (NO) and an increase in the production of vasoconstrictors such as Endothelin-1 (ET-1). NO is an important vasodilator that regulates vascular tone and maintains the integrity of the endothelial barrier. The reduction in NO production leads to vasoconstriction and increased permeability of the pulmonary capillaries. ET-1, on the other hand, is a potent vasoconstrictor that promotes inflammation and oxidative stress [3].

Oxidative stress is another important factor in the pathogenesis of NPE. It is characterized by an imbalance between the production of reactive oxygen species (ROS) and the antioxidant defence system. ROS are highly reactive molecules that can damage cellular membranes, proteins, and DNA [4]. The production of ROS is increased in various CNS disorders, and it can lead to endothelial dysfunction, inflammation, and increased permeability of the pulmonary capillaries.

Several preclinical studies have shown the potential of targeting endothelial dysfunction and oxidative stress as new therapeutic approaches for NPE. For example, the administration of NO donors or ET-1 antagonists has been shown to reduce pulmonary edema and improve respiratory function in animal models of NPE. In addition, the administration of antioxidants such as N-acetylcysteine (NAC) or resveratrol has been shown to reduce oxidative stress and improve pulmonary function in animal models of NPE [5].

However, there are several challenges to the development of new therapeutic approaches for NPE. First, the pathogenesis of NPE is complex, and it involves multiple factors. Therefore, targeting a single pathway may not be sufficient to achieve a significant therapeutic effect. Second, the translation of preclinical findings to clinical practice is often difficult, and many promising therapies fail in clinical trials. Third, the safety and efficacy of new therapies need to be carefully evaluated in clinical trials to avoid potential adverse effects.

Conclusion

Targeting endothelial dysfunction and oxidative stress are promising new therapeutic approaches for NPE. Preclinical studies have shown the potential of these approaches, and clinical trials are needed to evaluate their safety and efficacy. NPE is a life-threatening condition that requires urgent medical attention, and the development of new therapies is essential to improve the outcomes of patients with this complication.

References

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