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- W1820100522 abstract "Introduction: Pulmonary arterial hypertension (PAH) is characterized by increased vascular tone and remodeling of pulmonary vasculature. Imatinib- a potent inhibitor of tyrosine kinases, reverses pulmonary vascular remodeling in animal models of PAH and improves haemodynamics in selected PAH patients. However, the efficacy of long-term Imatinib administration on pulmonary arteriopathy and impaired vascular perfusion observed in severe PAH patients is not known. Aims: To examine the effects of long-term Imatinib (100mg/kg, PO QD) treatment on hemodynamics, and vascular perfusion in a severe preclinical rat model of PAH. Methods: Wistar Kyoto rats were treated once with SU5416 (20mg/kg, s.c.) and exposed to hypoxic conditions for 2 weeks (+ controls), + 8 weeks normoxia, + 4 weeks imatinib treatment (100mg/kg, q.d.). Haemodynamic parameters were analysed to determine extent of PAH pathology. Perfusion mapping was performed via lung vascular corrosion casts. Results : Rats exposed to chronic hypoxia/SU5416 developed severe right ventricular pressure (RVP >94mmHg) with decline in cardiac output (CO; -10.18 ml/min) compared to normoxic controls.Treatment with imatinib reduced all measures of PAH pathology (RVP ≤71 mmHg, CO; 6.42 ml/min). Macroscopic analysis of lung corrosion casts showed a large rarefaction of terminal branches of pulmonary vasculature (vascular pruning). Imatinib treatment greatly attenuated this decline. Conclusion: The above data further supports the beneficial effects of imatinib on PAH pathology. We show for the first time that Imatinib restores pulmonary vascular perfusion in a clinically relevant model of advanced PAH." @default.
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- W1820100522 date "2012-09-01" @default.
- W1820100522 modified "2023-09-27" @default.
- W1820100522 title "Effect of long-term imatinib treatment in a severe preclinical PAH rat model: An insight into pulmonary perfusion using a novel casting method" @default.
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