semaxinib and Pulmonary-Embolism

semaxinib has been researched along with Pulmonary-Embolism* in 1 studies

Other Studies

1 other study(ies) available for semaxinib and Pulmonary-Embolism

Article	Year
Chronic Embolic Pulmonary Hypertension Caused by Pulmonary Embolism and Vascular Endothelial Growth Factor Inhibition. The American journal of pathology, 2017, Volume: 187, Issue:4 Our understanding of the pathophysiological basis of chronic thromboembolic pulmonary hypertension (CTEPH) will be accelerated by an animal model that replicates the phenotype of human CTEPH. Sprague-Dawley rats were administered a combination of a single dose each of plastic microspheres and vascular endothelial growth factor receptor antagonist in polystyrene microspheres (PE) + tyrosine kinase inhibitor SU5416 (SU) group. Shams received volume-matched saline; PE and SU groups received only microspheres or SU5416, respectively. PE + SU rats exhibited sustained pulmonary hypertension (62 ± 13 and 53 ± 14 mmHg at 3 and 6 weeks, respectively) with reduction of the ventriculoarterial coupling in vivo coincident with a large decrement in peak rate of oxygen consumption during aerobic exercise, respectively. PE + SU produced right ventricular hypokinesis, dilation, and hypertrophy observed on echocardiography, and 40% reduction in right ventricular contractile function in isolated perfused hearts. High-resolution computed tomographic pulmonary angiography and Ki-67 immunohistochemistry revealed abundant lung neovascularization and cellular proliferation in PE that was distinctly absent in the PE + SU group. We present a novel rodent model to reproduce much of the known phenotype of CTEPH, including the pivotal pathophysiological role of impaired vascular endothelial growth factor-dependent vascular remodeling. This model may reveal a better pathophysiological understanding of how PE transitions to CTEPH in human treatments. Topics: Animals; Cardiomegaly; Cell Proliferation; Chronic Disease; Heart Function Tests; Hemodynamics; Hyperplasia; Hypertension, Pulmonary; Hypoxia; Indoles; Ki-67 Antigen; Lung; Male; Microspheres; Oxygen Consumption; P-Selectin; Partial Pressure; Physical Conditioning, Animal; Plasminogen Activator Inhibitor 1; Polystyrenes; Pulmonary Embolism; Pyrroles; Rats, Sprague-Dawley; Tissue Inhibitor of Metalloproteinase-1; Vascular Endothelial Growth Factor A; Ventricular Dysfunction	2017

Article

Year

Chronic Embolic Pulmonary Hypertension Caused by Pulmonary Embolism and Vascular Endothelial Growth Factor Inhibition.

The American journal of pathology, 2017, Volume: 187, Issue:4

Our understanding of the pathophysiological basis of chronic thromboembolic pulmonary hypertension (CTEPH) will be accelerated by an animal model that replicates the phenotype of human CTEPH. Sprague-Dawley rats were administered a combination of a single dose each of plastic microspheres and vascular endothelial growth factor receptor antagonist in polystyrene microspheres (PE) + tyrosine kinase inhibitor SU5416 (SU) group. Shams received volume-matched saline; PE and SU groups received only microspheres or SU5416, respectively. PE + SU rats exhibited sustained pulmonary hypertension (62 ± 13 and 53 ± 14 mmHg at 3 and 6 weeks, respectively) with reduction of the ventriculoarterial coupling in vivo coincident with a large decrement in peak rate of oxygen consumption during aerobic exercise, respectively. PE + SU produced right ventricular hypokinesis, dilation, and hypertrophy observed on echocardiography, and 40% reduction in right ventricular contractile function in isolated perfused hearts. High-resolution computed tomographic pulmonary angiography and Ki-67 immunohistochemistry revealed abundant lung neovascularization and cellular proliferation in PE that was distinctly absent in the PE + SU group. We present a novel rodent model to reproduce much of the known phenotype of CTEPH, including the pivotal pathophysiological role of impaired vascular endothelial growth factor-dependent vascular remodeling. This model may reveal a better pathophysiological understanding of how PE transitions to CTEPH in human treatments.

Topics: Animals; Cardiomegaly; Cell Proliferation; Chronic Disease; Heart Function Tests; Hemodynamics; Hyperplasia; Hypertension, Pulmonary; Hypoxia; Indoles; Ki-67 Antigen; Lung; Male; Microspheres; Oxygen Consumption; P-Selectin; Partial Pressure; Physical Conditioning, Animal; Plasminogen Activator Inhibitor 1; Polystyrenes; Pulmonary Embolism; Pyrroles; Rats, Sprague-Dawley; Tissue Inhibitor of Metalloproteinase-1; Vascular Endothelial Growth Factor A; Ventricular Dysfunction

2017