Pulmonary Vascular Remodeling in Rats Following Methamphetamine Self-Administration: Toward a Model of Methamphetamine-Associated Pulmonary Arterial Hypertension

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ID: 316860
2026
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Ranked #122 of 124 articles by views in toxicological sciences : an official journal of the society of toxicology

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Abstract
Abstract Background Pulmonary arterial hypertension (PAH) is a progressive vasculopathy characterized by pulmonary vascular remodeling. Methamphetamine (MA) exposure is strongly associated with PAH in humans, yet prior animal models rely on fixed, non-contingent dosing that does not replicate binge/crash patterns of human MA use. This study introduces an intravenous MA self-administration model to evaluate pulmonary vascular and cardiac consequences of human-like MA exposure. Methods Sixteen male Wistar rats underwent an 8-week protocol in which eight rats self-administered MA and eight yoked-saline controls received volume-matched saline. MA intake, lever-press behavior, and binge/crash dynamics were quantified. Lungs and hearts were harvested for histology, immunofluorescence, medial wall thickness quantification across vessel sizes, ventricular weights, and Fulton index. Results MA-exposed rats demonstrated escalating intake, with daily self-administered doses increasing from early-week values to a cumulative exposure of 526.7 ± 217.8 mg/kg over eight weeks. Distinct binge-and-crash patterns emerged as intake escalated over the exposure period. Compared with controls, MA-exposed rats exhibited pulmonary vascular remodeling predominantly in distal vessels, including medial hypertrophy, increased muscularization of small arterioles, and focal endothelial proliferation. Additional airway-centered parenchymal changes were observed in a subset of MA rats. No significant differences were found in right or left ventricular weights or Fulton index. Conclusion Chronic MA self-administration induces early pulmonary vascular remodeling without cardiac hypertrophy, indicating that this behaviorally relevant model captures early pulmonary vascular changes relevant to MA-associated pulmonary vascular disease. This model provides a translational platform for investigating MA-induced pulmonary vascular injury and identifying therapeutic targets.
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Authors Prangthip Charoenpong, Nicole M Hall, Courtney M. Keller, Ashok Kumar, Ling Chen, J. Gatuz, Najam Siddiqui, Fereshteh Sadat Tabatabaei Yazdi, Daffolyn Rachael Fels Elliott, Navneet K. Dhillon, Kevin S. Murnane, Nicholas E. Goeders, Robert Walter
Journal toxicological sciences : an official journal of the society of toxicology
Year 2026
DOI
10.1093/toxsci/kfag072
URL
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