Effects of ibuprofen on pulmonary oedema in an animal smoke inhalation model

Stewart, RJ; Yamaguchi, Kent T.; Knost, PM; Mason, SW; Roshdieh, BB; Samadani, S.; Chang, Boyang

doi:10.1016/0305-4179(90)90067-7

Cited by 9 publications

(2 citation statements)

References 18 publications

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“…The death rate for patients with inhalation injuries was 69.90% compared to 6.45% in patients without inhalation injury, emphasizing that inhalation injury is a predictive factor in mortality of burns [20]. Although the exact mechanism for respiratory complications of inhalation injury and/or burn has not been defined, different mechanisms are postulated by many authors; [21] & [22] attributed them to a combination of thermal, hypoxaemic and chemical effects of smoke. Billi et al, [3] mentioned the role of neutrophil implicated acute inflammatory process, while [23] reported the role of carbon monoxide, noxious gases and free radical generations; so this work was designed to detect the effect of smoke inhalation injury or\ and burn on lung histopathology and on antioxidants levels.…”

Section: Discussionmentioning

confidence: 99%

Inhalation injury and burn trauma: an experimental investigation of oxidative stress and histopathology

Eshak¹,

Nasef²

2013

Scandinavian Journal of Forensic Science

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Smoke inhalation injury is associated with high incidence of pulmonary complications as it represents a major cause of mortality after major burn injury. Burn is associated with release of inflammatory mediators which ultimately cause local and distant pathophysiological effects. The present study investigated the effect of smoke inhalation or\and burn injury on the antioxidants status in the lungs in a rat model to simulate an inhalation injury as might be encountered by firefighters and burn victims. Seventy five rats were equally randomized to five groups: Sham group, smoke inhalation injury group, burn group, sham burn group, and smoke burn group. At the end of the exposure protocol rats were killed by cervical decapitation and the lungs were removed completely and processed for histopathological and biochemical analysis by measuring lung antioxidant enzyme activities: Malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPs) level, as an index of lipid peroxidation. Grossly, results showed that rats´lungs in the smoke inhalation group and the smoke burn group showed multiple hemorrhagic spots. Light microscopic examination showed localized and diffuse alveolar hemorrhage. Two rats in the burn group had evidence of pneumonia and lung abscesses. Biochemically, results showed that both smoke inhalation and burn injury significantly elevated lung MDA and glutathione peroxidase levels when compared with controls. The combined smoke and burn group resulted in a more significant rise in both antioxidant levels indicating a higher level of lipid peroxidation. SOD level was significantly lowered on exposure to both conditions when compared to control. SOD level was significantly lower in the combined injury group when compared to either smoke or burn alone. In conclusion; the above data provide evidence that inhalation injury with and without burn decrease tissue antioxidant capacity and increase tissue peroxidative injury.

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Section: Discussionmentioning

confidence: 99%

Inhalation injury and burn trauma: an experimental investigation of oxidative stress and histopathology

Eshak¹,

Nasef²

2013

Scandinavian Journal of Forensic Science

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“…Currently, I BU is available as an over-the-counter nonprescription antipyretic and analgesic medicine. IBU, a cyclooxygenase inhibitor, has been shown to be efficacious in several acute lung injury models such as smoke inhalation (Stewart et al, 1990;Shinoza et al, 1986), paraquat (Lindenschmidt et al, 1983), and acid aspiration (Utsunomiya et al, 1982). IBU has also been examined successfully in previous phosgene inhalation models Sciuto et al, 1996b).…”

mentioning

confidence: 99%

Ibuprofen Treatment Enhances the Survival of Mice Following Exposure to Phosgene

Sciuto

1997

Inhalation Toxicology

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The present study was designed to investigate the efficacy of ibuprofen ( IBU) administered after a lethal dose of phosgene. Mice were exposed to 32 mg/m 3 phosgene for 20 min and immediately injected with IBU ( 0, 3, 9, or 15 mg/mouse, ip) . Five hours later, a second IBU injection was given but at half the original doses ( 0, 1.5, 4.5, and 7.5 mg/mouse). These are referred to throughout as the 0/ 0, 3/ 1. 5, 9/ 4.5, and 15/7.5 mg IBU/ mouse groups. Survival in these groups was determined at 12 and 24 h. In mice that died within 12 h, the lungs were removed, and lung wet weights, dry weights, wet/ dry weight ratios, malondialdedyde (MDA) , and nonprotein sulfhydryls ( NPSH) were measured. Survival odds ratios were calculated for each dose at 12 and 24 h. The 12-h survival was 63% for 9/ 4.5 mg IBU and 82% for the 15/7.5 mg IBU group compared with 25% for saline-treated mice. At 24 h, survival rates were reduced to 19% , 19%, and 6% , respectively. In the 15/7.5 mg IBU group, dry weights, wet/ dry weight ratios, and wet weights were significantly lower than in saline-treated mice at 12 h. MDA was lower only for the 9/ 4.5 mg IBU dose; however, NPSHs were greater across all IBU doses. The survival odds ratio was 5 for the 9/ 4.5 IBU group at 12 h and 13 for the 15/7.5 mg IBU group compared with 3.5 for both groups at 24 h. Therefore, IBU treatment increased the survival of mice at 12 h by reducing edema formation, lipid peroxidation, and glutathione depletion.

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Respiratory System

Radi

2012

Comparative Pathophysiology and Toxicology of Cyclooxygenases

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Effects of ibuprofen on pulmonary oedema in an animal smoke inhalation model

Cited by 9 publications

References 18 publications

Inhalation injury and burn trauma: an experimental investigation of oxidative stress and histopathology

Inhalation injury and burn trauma: an experimental investigation of oxidative stress and histopathology

Ibuprofen Treatment Enhances the Survival of Mice Following Exposure to Phosgene

Respiratory System

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