Monocrotaline pyrrole induces pulmonary endothelial damage through binding to and release from erythrocytes in lung during venous blood reoxygenation
العنوان: | Monocrotaline pyrrole induces pulmonary endothelial damage through binding to and release from erythrocytes in lung during venous blood reoxygenation |
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المؤلفون: | Zhi-Cheng Jing, Jiansha Li, Yuan Su, Qinghua Hu, Liping Zhu, Tao Wang, Rui Xiao, Yankai Lu, Jiwei Zhang, Shengquan Luo, Jocelyn Dupuis, Jing Fang |
المصدر: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 316:L798-L809 |
بيانات النشر: | American Physiological Society, 2019. |
سنة النشر: | 2019 |
مصطلحات موضوعية: | Pulmonary and Respiratory Medicine, Erythrocytes, Monocrotaline, Lung, Physiology, Chemistry, Hypertension, Pulmonary, Endothelial Cells, Cell Biology, Venous blood, Pharmacology, medicine.disease, Pulmonary hypertension, Rats, Oxygen, Rats, Sprague-Dawley, Animal model, medicine.anatomical_structure, Physiology (medical), Monocrotaline pyrrole, medicine, Animals, Endothelium |
الوصف: | Monocrotaline has been widely used to establish an animal model of pulmonary hypertension, most frequently in rats. An important feature of this model resides in the selectivity of monocrotaline injury toward the pulmonary vascular endothelium versus the systemic vasculature when administrated at standard dosage. The toxic metabolite of monocrotaline, monocrotaline pyrrole, is transported by erythrocytes. This study aimed to reveal whether partial pressure of oxygen of blood determined the binding and release of monocrotaline pyrrole from erythrocytes in rats with one subcutaneous injection of monocrotatline at the standard dosage of 60 mg/kg. Our experiments demonstrated that monocrotaline pyrrole bound to and released from erythrocytes at the physiological levels of partial pressure of oxygen in venous and arterial blood, respectively, and then aggregated on pulmonary artery endothelial cells. Monocrotaline pyrrole-induced damage of endothelial cells was also dependent on partial pressure of oxygen. In conclusion, our results demonstrate the importance of oxygen partial pressure on monocrotaline pyrrole binding to erythrocytes and on aggregation and injury of pulmonary endothelial cells. We suggest that these mechanisms contribute to pulmonary selectivity of this toxic injury model of pulmonary hypertension. |
تدمد: | 1522-1504 1040-0605 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::72f477d8bf4b0656cf7814629bba77ab https://doi.org/10.1152/ajplung.00279.2018 |
حقوق: | OPEN |
رقم الأكسشن: | edsair.doi.dedup.....72f477d8bf4b0656cf7814629bba77ab |
قاعدة البيانات: | OpenAIRE |
تدمد: | 15221504 10400605 |
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