VI. Electrocardiographic Study of Heart and Effect of Vagotomy in Phosgene Poisoning.

Bruner, H. D.; Boche, R; Gibbon, Mary H.; McCarthy, Miles D.

doi:10.3181/00379727-68-16455

Cited by 7 publications

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“…Accordingly, the activation of nerve afferents—either by chemical irritants or by physical stresses—may have elicited the respiratory and cardiovascular reflex responses shown in Figs. 1 and 2 [78–82]. This striking coherence was also demonstrated by the increased Penh proportional to the length of the apnea period (Figs.…”

Section: Experimental Studiessupporting

confidence: 54%

“…This process may have aggravated the acute edema and anoxic anoxia in the accompanying hemodynamic state of increasing hemoconcentration and blood viscosity. All of these factors, including those caused by intense vagus stimulation [82, 86, 87], seriously impede gas exchange and further lead to imbalances in the fluid dynamics of the lung. Collectively, cardiovascular disturbances (cardiogenic edema caused by imbalanced Starling forces), rather than an appreciable disruption of the air‐blood barrier function, were believed to be the predominant etiopathology of the phosgene‐induced lung edema (at this Cxt).…”

Section: Experimental Studiesmentioning

confidence: 99%

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Phosgene‐induced acute lung injury (ALI): differences from chlorine‐induced ALI and attempts to translate toxicology to clinical medicine

Pauluhn

2017

Clinical & Translational Med

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BackgroundPhosgene (carbonyl dichloride) gas is an indispensable chemical inter‐mediate used in numerous industrial processes. There is no clear consensus as to its time‐ and inhaled‐dose‐dependent etiopathologies and associated preventive or therapeutic treatment strategies. MethodsCardiopulmonary function was examined in rats exposed by inhalation to the alveolar irritant phosgene or to the airway irritant chlorine during and following exposure. Terminal measurements focused on hematology, protein extravasation in bronchoalveolar lavage (BAL), and increased lung weight. Noninvasive diagnostic and prognostic endpoints in exhaled breath (carbon dioxide and nitric oxide) were used to detect the clinically occult stage of pulmonary edema. ResultsThe first event observed in rats following high but sublethal acute exposure to phosgene was the stimulation of alveolar nociceptive vagal receptors. This afferent stimulation resulted in dramatic changes in cardiopulmonary functions, ventilation: perfusion imbalances, and progressive pulmonary edema and phospholipoproteinosis. Hematology revealed hemoconcentration to be an early marker of pulmonary edema and fibrin as a discriminating endpoint that was positive for the airway irritant chlorine and negative for the alveolar irritant phosgene. ConclusionsThe application of each gas produced typical ALI/ARDS (acute lung injury/acute respiratory distress syndrome) characteristics. Phosgene‐induced ALI showed evidence of persistent apnea periods, bradycardia, and shifts of vascular fluid from the peripheral to the pulmonary circulation. Carbon dioxide in expired gas was suggestive of increased ventilation dead space and appeared to be a harbinger of progressively developing lung edema. Treatment with the iNOS inhibitor aminoguanidine aerosol by inhalation reduced the severity of phosgene‐induced ALI when applied at low dose‐rates. Symptomatic treatment regimens were considered inferior to causal modes of treatment.

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Section: Experimental Studiessupporting

confidence: 54%

Section: Experimental Studiesmentioning

confidence: 99%