Free radicals mediate amphetamine-induced acute pulmonary edema in isolated rat lung

Huang, Kunlun; Shaw, Kai-Ping; Wang, David; Hsu, Kang; Huang, Tze-Shung; Chen, Hsing-I

doi:10.1016/s0024-3205(02)01847-7

Cited by 18 publications

(8 citation statements)

References 19 publications

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“…The involvement of proinflammatory cytokines and free radicals in septic shock and other disorders with organ dysfunctions including lung injury has been well documented [18,[31][32][33]. Recent clinical and laboratory investigations further supported the importance of cytokines and vascular adhesion molecules in acute lung injury.…”

Section: Discussionmentioning

confidence: 97%

The detrimental role of inducible nitric oxide synthase in the pulmonary edema caused by hypercalcemia in conscious rats and isolated lungs

2007

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We aim to test the hypothesis that hypercalcemia produces pulmonary edema (PE) and to elucidate the mechanism. Experimentations were carried out in conscious rats and isolated perfused rat lungs. We evaluated PE by lung weight changes, protein concentration in bronchoalveolar lavage, dye leakage, and microvascular permeability. Plasma nitrate/nitrite, methyl guanidine (MG), proinflammatory cytokines, procalcitonin levels, and histopathological examinations were evaluated. Immunochemical staining and reverse-transcriptase polymerase chain reaction (RT-PCR) were used to detect inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) in the lungs. Hypercalcemia was produced in the conscious rat and isolated perfused lungs. Calcitonin and L-N(6) (1-iminoethyl)-lysine (L-Nil) were administered before hypercalcemia to observe their effects. Hypercalcemia caused severe PE in rats. Pathological and immunochemical examinations revealed hemorrhagic edema with iNOS activity in the alveolar macrophages and epithelial cells. RT-PCR showed an increase in iNOS mRNA expression. Hypercalcemia increased nitrate/nitrite, MG, proinflammatory cytokines and procalcitonin levels. Pretreatment with calcitonin or L-Nil prevented these changes. In conclusion, hypercalcemia caused PE in conscious rats and isolated perfused rat lungs. The increases in nitrate/nitrite, free radicals, proinflammatory cytokines, procalcitonin and iNOS activity suggest that hypercalcemia induces a sepsis-like syndrome. The effect of hypercalcemia on the lung may involve iNOS and NO.

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Section: Discussionmentioning

confidence: 97%

The detrimental role of inducible nitric oxide synthase in the pulmonary edema caused by hypercalcemia in conscious rats and isolated lungs

2007

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“…Furthermore, Huang et al demonstrated that free radicals mediate amphetamine-induced acute pulmonary edema in isolated rat lung (Huang et al, 2002). Therefore, it is reasonable to suggest that in the model reported here, increased free radical formation results in cellular toxicity contributing to pulmomary edema.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, there is evidence that free radicals may play a role in amphetamine-related lung injury. In an isolated rat lung model, Huang et al demonstrated that the injury observed following amphetamine administration was associated with overproduction of free radicals (Huang et al, 2002). Although most of the reported side effects of smoking MA have been systemic, case reports of pulmonary complications including acute noncardiogenic pulmonary edema (Nestor et al, 1989a, 1989b) and fatal pulmonary hypertension (Schaiberger et al, 1993) have been reported.…”

mentioning

confidence: 99%

Acute Inhalation Exposure to Vaporized Methamphetamine Causes Lung Injury in Mice

Wells¹,

Buford²,

Braseth³

et al. 2008

Inhalation Toxicology

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Methamphetamine (MA) is currently the most widespread illegally used stimulant in the United States. Use of MA by smoking is the fastest growing mode of administration, which increases concerns about potential pulmonary and other medical complications. A murine exposure system was developed to study the pulmonary affects of inhaled MA. Mice were exposed to 25-100 mg vaporized MA and assessments were made 3 h following initiation of exposure to model acute lung injury. Inhalation of MA vapor resulted in dose-dependent increases in MA plasma levels that were in the range of those experienced by MA users. At the highest MA dose, histological changes were observed in the lung and small but significant increases in lung wet weight to body weight ratios (5.656 ± 0.176 mg/g for the controls vs. 6.706± 0.135 mg/g for the 100 mg MA-exposed mice) were found. In addition, there was 53% increase in total protein in bronchoalveolar lavage (BAL) fluid, greater than 20% increase in albumin levels in the BAL fluid, greater than 2.5-fold increase in lactate dehydrogenase levels in the BAL fluid, and reduced total BAL cell numbers (approximately 77% of controls). Levels of the early response cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-6 were dose-dependently increased in BAL fluid of MA-exposed mice. Exposure to 100 mg MA significantly increased free radical generation in the BAL cells to 107-146% of controls and to approximately 135% of the controls in lung tissue in situ. Together, these data show that acute inhalation exposure to relevant doses of volatilized MA is associated with elevated free radical formation and significant lung injury.Methamphetamine hydrochloride (MA) is a substituted amphetamine with potent central nervous system stimulant effects, and is currently the most widespread illegally used stimulant in the United States (NIDA, 2006). Like cocaine, MA can be snorted, injected, ingested, or smoked. According to the 2007 National Drug Threat Assessment Report by the National Drug Intelligence Center, smoking is the fastest growing primary mode of administration. From 1993 to 2004, use of MA by smoking grew from 15% to nearly 60% (NDIC, 2006). Smoking MA may result in more rapid addiction to the drug than snorting or injection because smoking causes a nearly instantaneous, intense, and longer lasting high (NIDA, 2002 may lead to increased rates of addiction that will further strain the resources of public health agencies.Studies of other inhaled drugs including marijuana and cocaine have shown that these substances can cause a variety of pulmonary complications. Chronic marijuana use is associated with increased prevalence of symptoms of chronic bronchitis, including chronic cough, sputum production, wheeze, and increased outpatient visits for respiratory illness (Bloom et al., 1987;Tashkin et al., 1987;Taylor et al., 2000;Taylor et al., 2002). Marijuana use also affects airway pathology by causing lower-airway injury, inflammation, and impairment in the antimicrobial and tumoricidal funct...

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“…[16,[79][80][81] In addition, amphetamine, phorbal myristate acetate, oleic acid have been employed for the induction of ALI. [82][83][84][85][86] Phorbol myristate acetate (PMA, 12-O-tetradecanoyl-phorbol-13-acetate), an ester derivative from croton oil has been used to induce ALI. [65,83,86,87] Experiments in vivo and in vitro have demonstrated that PMA is a strong neutrophil activator.…”

Section: Risk Factors and Pathogenetic Mechanismsmentioning

confidence: 99%

Acute lung injury and acute respiratory distress syndrome: experimental and clinical investigations

Chen¹

2011

Journal of Geriatric Cardiology

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Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) can be associated with various disorders. Recent investigation has involved clinical studies in collaboration with clinical investigators and pathologists on the pathogenetic mechanisms of ALI or ARDS caused by various disorders. This literature review includes a brief historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the long-term experimental studies and clinical investigations from our laboratory, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS.

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Free radicals mediate amphetamine-induced acute pulmonary edema in isolated rat lung

Cited by 18 publications

References 19 publications

The detrimental role of inducible nitric oxide synthase in the pulmonary edema caused by hypercalcemia in conscious rats and isolated lungs

The detrimental role of inducible nitric oxide synthase in the pulmonary edema caused by hypercalcemia in conscious rats and isolated lungs

Acute Inhalation Exposure to Vaporized Methamphetamine Causes Lung Injury in Mice

Acute lung injury and acute respiratory distress syndrome: experimental and clinical investigations

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