Adjuvant use of warm butyl alcohol vapor in experimental pulmonary edema

Waugh, William H.

doi:10.1016/0024-3205(93)90137-r

Cited by 2 publications

(2 citation statements)

References 24 publications

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“…However, simple oxygen therapy would not achieve adequate effects on alveolar edema clearance. Ethanol/butanol-oxygen vapor therapy (oxygen inhalation with 20% ethanol or butanol as humidifying agent) is a common treatment to pulmonary edema with a long history of safety [72][73][74][75]. Ethanol/butanol vapor decreases the surface tension of the foam inside the pulmonary alveoli and therefore alleviating alveolar edema (Table 2) [72][73][74][75].…”

Section: Alveolar Edema In Covid-19mentioning

confidence: 99%

“…Ethanol/butanol-oxygen vapor therapy (oxygen inhalation with 20% ethanol or butanol as humidifying agent) is a common treatment to pulmonary edema with a long history of safety [72][73][74][75]. Ethanol/butanol vapor decreases the surface tension of the foam inside the pulmonary alveoli and therefore alleviating alveolar edema (Table 2) [72][73][74][75]. Moreover, conservative fluid management, in which diuretics may be administered and intravenous fluid administration is minimized, would reduce hydrostatic pressure and enhance serum oncotic pressure, and therefore limit the development of pulmonary edema potentially (Table 2) [76][77][78].…”

Section: Alveolar Edema In Covid-19mentioning

confidence: 99%

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The Role of Alveolar Edema in COVID-19

Yuan

Jiang

Zhang

et al. 2021

Cells

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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.

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Section: Alveolar Edema In Covid-19mentioning

confidence: 99%

Section: Alveolar Edema In Covid-19mentioning

confidence: 99%

The Role of Alveolar Edema in COVID-19

Yuan

Jiang

Zhang

et al. 2021

Cells

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Enhanced isoproterenol-induced cardiac hypertrophy in transgenic rats with low brain angiotensinogen

Campos¹,

Iliescu²,

Fontes³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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We have previously shown that a permanent deficiency in the brain renin-angiotensin system (RAS) may increase the sensitivity of the baroreflex control of heart rate. In this study we aimed at studying the involvement of the brain RAS in the cardiac reactivity to the beta-adrenoceptor (beta-AR) agonist isoproterenol (Iso). Transgenic rats with low brain angiotensinogen (TGR) were used. In isolated hearts, Iso induced a significantly greater increase in left ventricular (LV) pressure and maximal contraction (+dP/dt(max)) in the TGR than in the Sprague-Dawley (SD) rats. LV hypertrophy induced by Iso treatment was significantly higher in TGR than in SD rats (in g LV wt/100 g body wt, 0.28 +/- 0.004 vs. 0.24 +/- 0.004, respectively). The greater LV hypertrophy in TGR rats was associated with more pronounced downregulation of beta-AR and upregulation of LV beta-AR kinase-1 mRNA levels compared with those in SD rats. The decrease in the heart rate (HR) induced by the beta-AR antagonist metoprolol in conscious rats was significantly attenuated in TGR compared with SD rats (-9.9 +/- 1.7% vs. -18.1 +/- 1.5%), whereas the effect of parasympathetic blockade by atropine on HR was similar in both strains. These results indicate that TGR are more sensitive to beta-AR agonist-induced cardiac inotropic response and hypertrophy, possibly due to chronically low sympathetic outflow directed to the heart.

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Adjuvant use of warm butyl alcohol vapor in experimental pulmonary edema

Cited by 2 publications

References 24 publications

The Role of Alveolar Edema in COVID-19

The Role of Alveolar Edema in COVID-19

Enhanced isoproterenol-induced cardiac hypertrophy in transgenic rats with low brain angiotensinogen

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