Effects of Chronic Exposure to Crack Cocaine on the Respiratory Tract of Mice

Abstract

Smoked cocaine (crack cocaine) causes several forms of injury to the respiratory tract, including asthma exacerbations, lung edema and hemorrhage, and nasal mucosal alterations. Few studies, however, have assessed respiratory tract pathology in habitual users of crack cocaine. Here, we describe the histological alterations in the respiratory tract of mice caused by chronic inhalation of crack cocaine. Twenty 2-month-old BALB/c mice were exposed to the smoke of 5 g crack cocaine in an inhalation chamber once a day for two months and compared to controls (n ¼ 10). We then morphometrically analyzed nose and bronchiolar epithelial alterations, bronchiolar and alveolar macrophage cell density, alveolar hemosiderin content, and in addition determined the vasoconstriction index and the wall thickness of pulmonary arteries. The serum cocaine level was 212.5 ng/mL after a single inhalation. The mucus content of the nasal epithelium increased in crack-exposed animals, and the nasal and bronchial epithelium thickness decreased significantly. The alveolar hemosiderin content and the alveolar and bronchiolar macrophage cell density increased in animals exposed to crack. The vasoconstriction index increased in the pulmonary arteries of the exposed group. Chronic crack cocaine inhalation causes extensive histological changes along the entire respiratory tract.

Repeated inhalation of crack-cocaine affects spermatogenesis in young and adult mice

“…Indeed, a dose of 5 g of crack cocaine inhaled by the mice promotes a serum concentration of cocaine that would be similar to a nonlethal (safe for the cardiovascular system) dose of 0.69 to 1.37 mg/kg insufflated cocaine (Collins et al, 2007). Even in nonlethal doses there are pulmonary histological alterations in animals such as hemorrhage, nose and bronchial epithelium atrophy and macrophagic inflammation in the same exposure system that we use (Herculiani et al, 2009). The entrance of the crack cocaine in the body is inhaled (absorption by lungs) and that is why this drug is very addictive when compared to the injected or nosed cocaine, thus demonstrating that the dose applied in our study is consistent with a dose administered by users.…”

A new exposure model to evaluate smoked illicit drugs in rodents: A study of crack cocaine

“…The negative pressure allowed the use of less drug than required by other devices, and exposure to the smoke of 250 mg of crack cocaine achieved similar plasma cocaine concentrations as reported by Herculiani et al (2009) andPires et al (2012).…”

“…The main problems of the existing apparatus include the complexity of drug burning and smoke exposure (Boni, Barr, & Martin, 1991;Burchfield, Abrams, Miller, & DeVane, 1991;He, Lidow, & Lidow, 2006) and the large amount of drug that is required to perform the experiment (Herculiani et al, 2009). Therefore, this study developed an inexpensive and easily assembled apparatus for smoke exposure of inhaled drugs that requires small drug amounts that are safe for the researcher.…”

Computed tomographic assessment of airflow obstruction in smoke inhalation injury: Relationship with the development of pneumonia and injury severity

“…This study was an attempt to define the relationship of airway wall thickening with the severity of SII patients using chest CT in the early phase after injury [13]. An animal experimental study showed that the bronchial wall in mice with SII was expected to swell and be thicker than that in the control animals [14], and a correlation was also reported between bronchial wall thickness and airway narrowing using virtual bronchoscopy in a swine model [10]. However, no reports have evaluated this bronchial wall swelling with clinical data except in animal experiments [15].…”