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Bronchial artery ligation modifies pulmonary edema after exposure to smoke with acrolein.

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Pulmonary edema can follow smoke inhalation and is believed to be due to the multiple chemical toxins in smoke, not the heat. We have developed a synthetic smoke composed of aerosolized charcoal particles to which one toxin at a time can be added to determine whether it produces pulmonary edema.

Synthetic smoke with acrolein but not HCl produces pulmonary edema.

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The chemical toxins in smoke and not the heat are responsible for the pulmonary edema of smoke inhalation. We developed a synthetic smoke composed of carbon particles (mean diameter of 4.3 microns) to which toxins known to be in smoke, such as HCl or acrolein, could be added one at a time. We

BW-755C diminishes smoke-induced pulmonary edema.

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Pulmonary edema following smoke inhalation is due to the chemical toxins in smoke and not to the heat. We have shown that acrolein, a common component of smoke, induces pulmonary edema, perhaps via release of leukotrienes. We, therefore, hypothesized that acrolein, a component of smoke from burning

Smoke aldehyde component influences pulmonary edema.

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The pulmonary edema of smoke inhalation is caused by the toxins of smoke and not the heat. We investigated the potential of smoke consisting of carbon in combination with either acrolein or formaldehyde (both common components of smoke) to cause pulmonary edema in anesthetized sheep. Seven animals

Intrathecal cannabinoid-1 receptor agonist prevents referred hyperalgesia in acute acrolein-induced cystitis in rats.

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We investigated the capacity of intrathecal arachidonyl-2'-chloroethylamide (ACEA), a cannabinoid-1 receptor (CB1R) agonist, to inhibit referred hyperalgesia and increased bladder contractility resulting from acute acrolein-induced cystitis in rats. 24 female rats were divided into 4 groups: 1)

Fate and effects of acrolein.

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Acrolein is a highly toxic, reactive, and irritating aldehyde that occurs as a product of organic pyrolysis, as a metabolite of a number of compounds, and as a residue in water when used for the control of aquatic organisms. It is an intermediate in the production of acrylic acid, DL-methionine, and

Cyclooxygenase and lipoxygenase inhibition by BW-755C reduces acrolein smoke-induced acute lung injury.

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Inhalation of smoke containing acrolein, the most common toxin in urban fires after carbon monoxide, causes vascular injury with non-cardiogenic pulmonary edema containing potentially edematogenic eicosanoids such as thromboxane (Tx) B2, leukotriene (LT) B4, and the sulfidopeptide LTs (LTC4, LTD4,

Acrolein Aggravates Secondary Brain Injury After Intracerebral Hemorrhage Through Drp1-Mediated Mitochondrial Oxidative Damage in Mice

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Clinical advances in the treatment of intracranial hemorrhage (ICH) are restricted by the incomplete understanding of the molecular mechanisms contributing to secondary brain injury. Acrolein is a highly active unsaturated aldehyde which has been implicated in many nervous system diseases. Our

Subacute acrolein exposure to rat larynx in vivo.

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Inhaled pollutants can contact vocal fold tissue and induce detrimental voice changes. Acrolein is a pollutant in cigarette smoke and can also be inhaled during the combustion of fossil fuels, animal fats, and plastics in the environment. However, the vocal fold pathological changes

The impact of inhaled acrolein on hypertension-sensitive and resistant rats.

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The Dahl selected rat lines, one susceptible to salt-induced hypertension (DS) and the other resistant to salt-induced hypertension (DR), were subchronically exposed to filtered air, 0.4, 1.4, or 4.0 ppm acrolein. All of the DS rats exposed to 4.0 ppm acrolein died within the first 11 days, while

Selected responses of hypertension-sensitive and resistant rats to inhaled acrolein.

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The Dahl selected rat lines, one susceptible to salt-induced hypertension (DS) and the other resistant to salt-induced hypertension (DR), were exposed to filtered air, 0.4, 1.4, or 4.0 ppm acrolein for 6 h/day, 5 days/week for 62 days. All of the DS rats exposed to 4.0 ppm acrolein died within the

Endothelial dysfunction and claudin 5 regulation during acrolein-induced lung injury.

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An integral membrane protein, Claudin 5 (CLDN5), is a critical component of endothelial tight junctions that control pericellular permeability. Breaching of endothelial barriers is a key event in the development of pulmonary edema during acute lung injury (ALI). A major irritant in smoke, acrolein

Intermediate filament carbonylation during acute acrolein toxicity in A549 lung cells: functional consequences, chaperone redistribution, and protection by bisulfite.

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Extensive protein carbonylation accompanies cellular exposure to acrolein, a ubiquitous smoke constituent implicated in life-threatening pulmonary edema in fire victims, a condition involving rapid erosion of the "watertight" properties of respiratory epithelium. Since the identities of lung

Changes in rat lung structure and composition as a result of subchronic exposure to acrolein.

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Groups of Fischer-344 rats were exposed to either filtered air, 0.4, 1.4, or 4.0 ppm acrolein for 62 days (6 h/day, 5 days/week). Mortality was observed only in the 4.0 ppm chamber, where 32 of 57 male rats died, but none of the 8 exposed females died. The lungs of the 4.0 ppm group were heavier

[Pulmonary edema due to inhalation of gas and vapors].

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In 1975, France will have manufactured 3.2 million tons of plastic materials which by pyrolysis, liberate chlorine, methyl chloride, hydrocyanic acid, hydrofluoric acid and other toxic gases. Now these materials are burnt in fires in "modern", buildings or vehicles , associated with fats (acrolein)

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