Role of surfactant proteins in development of pulmonary edema

INTRODUCTION: The problem of pulmonary edema is relevant in the modern world, since despite significant progress in understanding the etiology, pathogenesis and approaches to treatment, mortality reaches 50%. The complexity and relevance of the problem are associated with differential diagnosis of cardiogenic and non-cardiogenic pulmonary edema, which is of principal significance in selection of treatment and diagnostic tactic. AIM: Based on the literature data, to analyze the diagnostic role of surfactant protein (SP) as a biomarker of pulmonary edema. Traditional analysis of cardiogenic pulmonary edema implies the development of high pressure in the pulmonary capillaries, which creates hydrostatic gradients for the flow of fluid from capillaries into the interstitial and alveolar spaces. Experimental studies were conducted on animals with modeled pulmonary edema, clinical studies of the pulmonary barrier dysfunction were conducted in patients with pulmonary edema. Studies on animal models show that high pressure in capillaries can cause disruption of the barrier in alveolar-capillary cells, which increases permeability and transport of fluid and protein into the lung parenchyma, with the subsequent dysfunction of surfactant. As reported in literature, some patients with cardiogenic pulmonary edema have elevated plasma levels of SP and tumor necrosis factor alpha, which reflects disruption of the barrier and acute tissue injury, respectively. Studies conducted in patients with chronic heart failure and impaired gas exchange have determined increase in the number of alveolar type II cells and increase in SP level in plasma. CONCLUSION: Thus, the conducted studies suggest that acute rise of capillary pressure can cause lung injury, destruct the barrier, and contribute to the overproduction of fluid both through hydrostatic mechanisms, and through alteration of the permeability of alveolar–capillary barrier. Upon that, patients with cardiogenic pulmonary edema had high SP levels in plasma.

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Publication Details

Journal
I P Pavlov Russian Medical Biological Herald
Published
2025-04-16
DOI
https://doi.org/10.17816/pavlovj568729
Primary Topic
Neonatal Respiratory Health Research
Type
article
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article

Role of surfactant proteins in development of pulmonary edema

Л. П. Воронина, Liya Pakhnova, Dmitry Pahnov
I P Pavlov Russian Medical Biological Herald
Neonatal Respiratory Health Research
article

Role of surfactant proteins in development of pulmonary edema

Л. П. Воронина, Liya Pakhnova, Dmitry Pahnov
article en

Abstract

INTRODUCTION: The problem of pulmonary edema is relevant in the modern world, since despite significant progress in understanding the etiology, pathogenesis and approaches to treatment, mortality reaches 50%. The complexity and relevance of the problem are associated with differential diagnosis of cardiogenic and non-cardiogenic pulmonary edema, which is of principal significance in selection of treatment and diagnostic tactic. AIM: Based on the literature data, to analyze the diagnostic role of surfactant protein (SP) as a biomarker of pulmonary edema. Traditional analysis of cardiogenic pulmonary edema implies the development of high pressure in the pulmonary capillaries, which creates hydrostatic gradients for the flow of fluid from capillaries into the interstitial and alveolar spaces. Experimental studies were conducted on animals with modeled pulmonary edema, clinical studies of the pulmonary barrier dysfunction were conducted in patients with pulmonary edema. Studies on animal models show that high pressure in capillaries can cause disruption of the barrier in alveolar-capillary cells, which increases permeability and transport of fluid and protein into the lung parenchyma, with the subsequent dysfunction of surfactant. As reported in literature, some patients with cardiogenic pulmonary edema have elevated plasma levels of SP and tumor necrosis factor alpha, which reflects disruption of the barrier and acute tissue injury, respectively. Studies conducted in patients with chronic heart failure and impaired gas exchange have determined increase in the number of alveolar type II cells and increase in SP level in plasma. CONCLUSION: Thus, the conducted studies suggest that acute rise of capillary pressure can cause lung injury, destruct the barrier, and contribute to the overproduction of fluid both through hydrostatic mechanisms, and through alteration of the permeability of alveolar–capillary barrier. Upon that, patients with cardiogenic pulmonary edema had high SP levels in plasma.

I P Pavlov Russian Medical Biological HeraldVol. 33(1)
Astrakhan State Medical University (RU)
Openalex Percentile: Top 79%
Neonatal Respiratory Health Research
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