Alterações morfofuncionais de artérias intrapulmonares de ratos Wistar após intoxicação crônica por 60 dias ao cloreto de mercúrio
Nenhuma Miniatura disponível
Data
2025-10-09
Autores
Schereider, Ingridy Reinholz Grafites
Título da Revista
ISSN da Revista
Título de Volume
Editor
Universidade Federal do Espírito Santo
Resumo
Mercury exposure is a significant public health concern due to its toxic potential in the human body, especially on the cardiovascular system. Its accumulation in the body induces oxidative stress, inflammation, and endothelial dysfunction in systemic arteries, contributing to the development of cardiovascular diseases. The close relationship between systemic and pulmonary circulation leads us to believe that the latter also suffers from the toxic effects of mercury. However, the consequences of HgCl₂ in the pulmonary arteries remain unclear. This study aimed to investigate the effects of mercury chloride (HgCl₂) exposure for 60 days on the small intrapulmonary arteries and hemodynamic parameters of male rats. The rats were exposed to HgCl₂ (1st dose, 4.6 μg/kg; subsequent daily doses, 0.07 μg/kg; intramuscular injection). The results revealed that intrapulmonary arteries from exposed rats exhibited reduced contractile responses to potassium chloride and the thromboxane A2 receptor agonist U46619, and arterial wall thinning, indicative of vascular hypotrophic remodeling. The impaired pulmonary vasoconstriction of the HgCl2 group was associated with increased nitric oxide (NO) and hydrogen peroxide (H₂O₂) levels. In addition, increased production of superoxide anion (O₂•-) and reduced superoxide dismutase (SOD) expressions. These findings suggest that chronic HgCl2 exposure induces pulmonary vascular dysfunctions, primarily through enhanced NO and ROS signaling as an adaptive mechanism against oxidative stress
Descrição
Palavras-chave
Artéria pulmonar , Mercúrio
, Estresse oxidativo , Disfunção endotelial , Reatividade vascular.