scholarly journals The Role of Alveolar Edema in COVID-19

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1897
Author(s):  
Shu Yuan ◽  
Si-Cong Jiang ◽  
Zhong-Wei Zhang ◽  
Yu-Fan Fu ◽  
Jing Hu ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Fluid Management ◽  
Exogenous Surfactant ◽  
Small Airways ◽  
Blood Oxygen ◽  
Blood Oxygen Saturation ◽  
Edema Fluid ◽  
One Year ◽  
Alveolar Edema

The coronavirus disease 2019 (COVID-19) has spread over the world for more than one year. COVID-19 often develops life-threateninghypoxemia. Endothelial injury caused by the viral infection leads to intravascular coagulation and ventilation–perfusion mismatch. However, besides above pathogenic mechanisms, the role of alveolar edema in the disease progression has not been discussed comprehensively. Since the exudation of pulmonary edema fluid was extremely serious in COVID-19 patients, we bring out a hypothesis that severity of alveolar edema may determine the size of poorly-ventilated area and the blood oxygen content. Treatments to pulmonary edema (conservative fluid management, exogenous surfactant replacementsand ethanol–oxygen vapor therapyhypothetically) may be greatly helpful for reducingthe occurrences of severe cases. Given that late mechanical ventilation may causemucus (edema fluid) to be blown deep intothe small airways,oxygentherapy should be given at the early stages. Theoptimaltimeand blood oxygen saturation (SpO2) thresholdforoxygentherapy are also discussed.

scholarly journals The Role of Alveolar Edema in COVID-19

2021 ◽  
Author(s):  
Shu Yuan ◽  
Si-Cong Jiang ◽  
Zi-Lin Li
Keyword(s):  
Pulmonary Edema ◽  
Oxygen Therapy ◽  
Fluid Management ◽  
Optimal Time ◽  
Small Airways ◽  
Edema Fluid ◽  
Life Threatening ◽  
One Year ◽  
Alveolar Edema

The coronavirus disease 2019 (COVID-19) has spread over the world for more than one year. COVID-19 often develops life-threatening hypoxemia. Endothelial injury caused by the viral infection leads to intravascular coagulation and ventilation-perfusion mismatch. However, besides above pathogenic mechanisms, the role of alveolar edema in the disease progression has not been discussed comprehensively. Since the exudation of pulmonary edema fluid was extremely serious in COVID-19 patients, we bring out a hypothesis that severity of alveolar edema may determine the size of poorly-ventilated area and the blood oxygen content. Treatments to pulmonary edema (alcohol-oxygen vapor therapy and fluid management) may be great helpful for reducing occurrence of severe cases. Given that late mechanical ventilation may cause mucus (edema fluid) to be blown to the deep of the small airways, oxygen therapy should be given at the early stages. The optimal time and SpO2 threshold for oxygen therapy are also discussed.

The role of menopause in the development of chronic mountain sickness

1997 ◽  
Vol 272 (1) ◽  
pp. R90-R94 ◽  
Author(s):  
F. Leon-Velarde ◽  
M. A. Ramos ◽  
J. A. Hernandez ◽  
D. De Idiaquez ◽  
L. S. Munoz ◽  
...  
Keyword(s):  
Premenopausal Women ◽  
Signs And Symptoms ◽  
Blood Oxygen ◽  
Blood Oxygen Saturation ◽  
Chronic Mountain Sickness ◽  
Female Population ◽  
Mountain Sickness ◽  
Cerro De Pasco ◽  
Expiratory Flow Rates

The objective of this study was to investigate the role of menopause in the appearance of the physiopathological sequence that leads to chronic mountain sickness (CMS) in a high-altitude female population. The females studied are 30-54 yr old (n = 152) and have permanent residence in Cerro de Pasco (Pasco, Peru; 4,300 m). The sample was divided into postmenopausal and premenopausal groups for comparison. Blood oxygen saturation (SaO2), excessive erythrocytosis [EE, measured by the level of hematocrit (Het)], peak expiratory flow rates (PEFR), and a score that represents the main signs and symptoms of CMS (CMSscore) were measured. Postmenopausal women had higher Het (50.2 +/- 4.04 vs. 47.4 +/- 4.13%, P < 0.001), lower SaO2 (81.9 +/- 4.12 vs. 84.7 +/- 3.14%, P < 0.001) and PEFR values (489 +/- 101 vs. 534 +/- 90 l/min, P < 0.02), and slightly higher CMSscore (19.1 +/- 3.37 vs. 17.9 +/- 3.48, P < 0.06) than premenopausal women. The prevalence of women with EE (EE = Hct > 56%) was found to be 8.8%. Forty-five percent of the postmenopausal subjects presented a high CMSscore (> 21), whereas only 22% of the premenopausal subjects presented this high value (P < 0.02). We can therefore conclude that menopause may represent a contributing factor for the development of CMS.

scholarly journals Inactivation of Exogenous Surfactant by Pulmonary Edema Fluid

1991 ◽  
Vol 29 (4) ◽  
pp. 353-356 ◽  
Author(s):  
Tsutomu Kobayashi ◽  
Keiko Nitta ◽  
Masaya Ganzuka ◽  
Sachiko Inui ◽  
Gertie Grossmann ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Exogenous Surfactant ◽  
Edema Fluid

scholarly journals Association of lipoprotein levels with sleep apnea: role of autonomic dysfunction

2021 ◽  
Vol 55 (1) ◽  
pp. 22-29
Author(s):  
Pavel Siarnik ◽  
Adela Penesova ◽  
Zofia Radikova ◽  
Alzbeta Hluchanova ◽  
Oto Hanus ◽  
...  
Keyword(s):  
Oxygen Saturation ◽  
Autonomic Dysfunction ◽  
Linear Regression Analysis ◽  
Area Under The Curve ◽  
Density Lipoprotein ◽  
Receiver Operating Curve ◽  
Blood Oxygen ◽  
Blood Oxygen Saturation ◽  
Significant Difference

Abstract Objectives. Although multiple mechanisms, including autonomic dysfunction, seem to link sleep-disordered breathing (SDB) with dyslipidemia in animal studies, the data in clinical studies are limited. The aim of this study was to explore the association of lipoprotein levels with SDB measures in healthy habitual snorers. We supposed that autonomic dysfunction is the linking mechanism. Methods. We enrolled 110 previously healthy subjects with complaints of habitual snoring. To assess SDB, polysomnography was performed. Blood samples for the analysis of total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein cholesterol (LDL), and triglycerides (TG) were obtained in a fasting condition after the polysomnography. Baroreflex sensitivity (BRS) was used to assess the autonomic dysfunction. Results. In stepwise multiple linear regression analysis, minimal nocturnal blood oxygen saturation (beta=–0.240, p=0.020) and neck circumference (beta=0.224, p=0.03) were the only significant contributors in model predicting TG. SDB measures were not identified as significant contributors in models predicting TC, LDL, and HDL. We failed to find any significant difference in BRS in SDB subjects when compared according to the presence or absence of hypercholesterolemia/ hypertriglyceridemia. In SDB subjects, the area under the curve in a receiver operating curve to predict hypercholesterolemia and hypertriglyceridemia by BRS was 0.468 (95% CI: 0.328–0.608) and 0.425 (95% CI: 0.304–0.546), respectively. Conclusions. Our results suggest that minimal nocturnal blood oxygen saturation is significant contributor in model predicting TG. No significant decrease in BRS was found in SDB subjects with hypercholesterolemia and hypertriglyceridemia. In SDB subjects, the role of autonomic dys-function in the development of dyslipidemia remains controversial.

scholarly journals Extracellular heat shock protein 72 is a marker of the stress protein response in acute lung injury

2006 ◽  
Vol 291 (3) ◽  
pp. L354-L361 ◽  
Author(s):  
Michael T. Ganter ◽  
Lorraine B. Ware ◽  
Marybeth Howard ◽  
Jérémie Roux ◽  
Brandi Gartland ◽  
...  
Keyword(s):  
Heat Shock ◽  
Pulmonary Edema ◽  
Stress Protein ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial ◽  
Edema Fluid ◽  
Protein Response ◽  
Alveolar Edema

Previous studies have shown that heat shock protein 72 (Hsp72) is found in the extracellular space (eHsp72) and that eHsp72 has potent immunomodulatory effects. However, whether eHsp72 is present in the distal air spaces and whether eHsp72 could modulate removal of alveolar edema is unknown. The first objective was to determine whether Hsp72 is released within air spaces and whether Hsp72 levels in pulmonary edema fluid would correlate with the capacity of the alveolar epithelium to remove alveolar edema fluid in patients with ALI/ARDS. Patients with hydrostatic edema served as controls. The second objective was to determine whether activation of the stress protein response (SPR) caused the release of Hsp72 into the extracellular space in vivo and in vitro and to determine whether SPR activation and/or eHsp72 itself would prevent the IL-1β-mediated inhibition of the vectorial fluid transport across alveolar type II cells. We found that eHsp72 was present in plasma and pulmonary edema fluid of ALI patients and that eHsp72 was significantly higher in pulmonary edema fluid from patients with preserved alveolar epithelial fluid clearance. Furthermore, SPR activation in vivo in mice and in vitro in lung endothelial, epithelial, and macrophage cells caused intracellular expression and extracellular release of Hsp72. Finally, SPR activation, but not eHsp72 itself, prevented the decrease in alveolar epithelial ion transport induced by exposure to IL-1β. Thus SPR may protect the alveolar epithelium against oxidative stress associated with experimental ALI, and eHsp72 may serve as a marker of SPR activation in the distal air spaces of patients with ALI.

scholarly journals Elevated VEGF Levels in Pulmonary Edema Fluid and PBMCs from Patients with Acute Hantavirus Pulmonary Syndrome

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Irina Gavrilovskaya ◽  
Elena Gorbunova ◽  
Frederick Koster ◽  
Erich Mackow
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Pulmonary Edema ◽  
Vascular Permeability ◽  
Hantavirus Pulmonary Syndrome ◽  
Acute Pulmonary Edema ◽  
Vascular Endothelial ◽  
Edema Fluid ◽  
Endothelial Growth Factor

Hantavirus pulmonary syndrome is characterized by vascular permeability, hypoxia, and acute pulmonary edema. Vascular endothelial growth factor (VEGF) is induced by hypoxia, potently induces vascular permeability, and is associated with high-altitude-induced pulmonary edema. Hantaviruses alter the normal regulation ofβ3 integrins that restrict VEGF-directed permeability and hantavirus infected endothelial cells are hyperresponsive to the permeabilizing effects of VEGF. However, the role of VEGF in acute pulmonary edema observed in HPS patients remains unclear. Here we retrospectively evaluate VEGF levels in pulmonary edema fluid (PEF), plasma, sera, and PBMCs from 31 HPS patients. VEGF was elevated in HPS patients PEF compared to controls with the highest levels observed in PEF samples from a fatal HPS case. VEGF levels were highest in PBMC samples during the first five days of hospitalization and diminished during recovery. Significantly increased PEF and PBMC VEGF levels are consistent with acute pulmonary edema observed in HPS patients and HPS disease severity. We observed substantially lower VEGF levels in a severe HPS disease survivor after extracorporeal membrane oxygenation. These findings suggest the importance of patients’ VEGF levels during HPS, support the involvement of VEGF responses in HPS pathogenesis, and suggest targeting VEGF responses as a potential therapeutic approach.

Oxidative stress and inflammation in COVID-19 pathogenesis

2020 ◽  
Vol 26 (4) ◽  
Author(s):  
Vladimir G. Kukes ◽  
Olga K. Parfenova ◽  
Nikita G. Sidorov ◽  
Yuri V. Olefir ◽  
Albina А. Gazdanova
Keyword(s):  
Oxidative Stress ◽  
Severe Acute Respiratory Syndrome ◽  
Oxygen Saturation ◽  
Viral Infections ◽  
Blood Oxygen ◽  
The Novel ◽  
Blood Oxygen Saturation ◽  
Metabolic Products ◽  
Respiratory Viral Infections

This study discusses the role of oxidative stress and inflammation in the development of severe acute respiratory syndrome (SARS) associated with COVID-19 caused by the novel SARS-CoV-2 coronavirus. An analysis of the literature revealed that the development of respiratory viral infections, including COVID-19, is usually accompanied by the accumulation of acidic metabolic products in the blood and tissues and, accordingly, oxidative stress and increased levels of cytokines. In this regard, it seems appropriate to use the second-generation low-toxic antioxidant Ethoxidol, manufactured in Russia, which reduces the intensity of inflammation, and also improves blood oxygen saturation.

scholarly journals Role of Blood Oxygen Saturation During Post-Natal Human Cardiomyocyte Cell Cycle Activities

2020 ◽  
Vol 5 (5) ◽  
pp. 447-460 ◽  
Author(s):  
Lincai Ye ◽  
Lisheng Qiu ◽  
Bei Feng ◽  
Chuan Jiang ◽  
Yanhui Huang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Oxygen Saturation ◽  
Blood Oxygen ◽  
Blood Oxygen Saturation

P1071WITHIN-PATIENT RELATIONSHIPS BETWEEN ULTRAFILTRATION AND FLUID GAINS IN HAEMODIALYSIS PATIENTS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Mai Nguyen ◽  
Richard Corbett ◽  
Neill Duncan ◽  
Damien Ashby
Keyword(s):  
Fluid Management ◽  
Dialysis Session ◽  
Patient Factors ◽  
Factors Affecting ◽  
Target Weight ◽  
One Year ◽  
Patient Relationships ◽  
Haemodialysis Treatment

Abstract Background and Aims Despite the now-widespread use of haemodialysis treatment, optimal fluid management in long-term dialysis patients remains challenging. Whilst the between-patient factors affecting target weight and ultrafiltration have been well studied, little is known regarding the within-patient factors affecting these relationships. Method Dialysis data for a group of stable haemodialysis patients, from 4 dialysis units, were analysed over a period of one year. All weights and volumes are expressed as percentage of target weight. Results From 100 patients (aged 28–89, mean 65.4, 54% male) observed over a year, complete data were available for 15530 dialysis sessions, and 13027 combinations of dialysis session plus the following inter-dialytic interval. Mean arterial pressure dropped by 3.5(+/-14.6)mmHg during dialysis, with a significant correlation (p&lt;0.05) between pressure drop and ultrafiltration volume in 26 patients (mean R=0.09, mean regression gradient 3.2). In 87 patients, inter-dialytic fluid gain correlated strongly (p&lt;0.05) with the previous dialysis session’s ultrafiltration volume (mean R=0.37, mean regression gradient 0.20) suggesting a significant role of ultrafiltration volume in driving subsequent fluid intake behaviour (thirst). Unsurprisingly, more fluid was gained over longer inter-dialytic intervals: mean(sd) weight at the start of dialysis was 103.2(1.0)% after a 3-day gap and 102.5(1.0)% after a 2-day gap, with this difference being significant (p&lt;0.05) in 87 patients. However, fluid gain was non-linear, diminishing during longer inter-dialytic intervals: mean(sd) daily inter-dialytic fluid gain was 1.13(0.38)% during the 3-day gap vs 1.21(0.53)% during the 2-day gap (p&lt;0.05 in 36 patients), implying that at least a third of patients consume less fluid during the 3rd post-dialysis day. Conclusion Inter-dialytic fluid gain is strongly dependent on ultrafiltration during the previous dialysis session, and diminishes during the inter-dialytic interval. Large ultrafiltration volumes, which have historically been perceived as the inevitable result of large fluid intakes, are actually a cause of thirst and large fluid intakes in haemodialysis patients. These data, derived from within-patient analyses, strongly challenge our conventional understanding of dialytic fluid management.

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