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<a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+BH&amp;cauthor_id=20670847" href="https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+BH&amp;cauthor_id=20670847" target="_blank" rel="noopener">B H Jiang</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Tardif+JC&amp;cauthor_id=20595149" href="https://pubmed.ncbi.nlm.nih.gov/?term=Tardif+JC&amp;cauthor_id=20595149" target="_blank" rel="noopener">J-C Tardif</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Shi+Y&amp;cauthor_id=20595149" href="https://pubmed.ncbi.nlm.nih.gov/?term=Shi+Y&amp;cauthor_id=20595149" target="_blank" rel="noopener">Y Shi,</a> <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Dupuis+J&amp;cauthor_id=20595149" href="https://pubmed.ncbi.nlm.nih.gov/?term=Dupuis+J&amp;cauthor_id=20595149" target="_blank" rel="noopener">J Dupuis</a>Affiliations ExpandPMID: 20595149 DOI: <a data-mce-href="https://doi.org/10.1183/09031936.00053710" href="https://doi.org/10.1183/09031936.00053710" target="_blank" rel="noopener">10.1183</a>/<a data-mce-href="https://doi.org/10.1183/09031936.00053710" href="https://doi.org/10.1183/09031936.00053710" target="_blank" rel="noopener" data-mce-selected="inline-boundary">09031936.00053710﻿</a> Free article<h2>Abstract</h2> Pulmonary hypertension (PH) and right ventricular (RV) dysfunction associated with heart failure (HF) carry a poor prognosis. Although endothelin receptor antagonists (ERAs) demonstrated benefits in pulmonary arterial hypertension, their efficacy in PH associated with HF was not specifically evaluated. 2 weeks after myocardial infarction (MI) rats received bosentan (100 or 200 mg·kg(-1)·day(-1)) or no treatment for 3 weeks. PH, RV hypertrophy and function as well as lung remodeling and function were evaluated. LV echocardiographic wall motion abnormality and function measured before treatment (2 weeks after MI) and after treatment (5 weeks after MI) were similar in MI control and MI treatment groups. HF induced PH and RV hypertrophy compared with sham: RV systolic pressure 39±5 versus 23±0.8 mmHg and RV/left ventricular+septum weight 52±7 versus 24±0.5% (all p&lt;0.01). Bosentan did not significantly modify these parameters. In addition, bosentan did not improve depressed RV function measured by echocardiograph from the RV myocardial performance index and tricuspid annular plane systolic excursion. The respiratory pressure-volume relationship revealed that HF caused a restrictive lung syndrome with histological lung remodeling and fibrosis, also not improved by bosentan. Dual ERA therapy with bosentan does not reduce PH, RV hypertrophy and lung remodeling and dysfunction associated with ischaemic HF.<a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/20595149/" href="https://pubmed.ncbi.nlm.nih.gov/20595149/" target="_blank" rel="noopener">Link</a>

Bosentan does not improve pulmonary hypertension and lung remodeling in heart failure

Human lungs healthcare and medical abstract background

<a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+BH&amp;cauthor_id=20670847" href="https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+BH&amp;cauthor_id=20670847" target="_blank" rel="noopener">Baohua Jiang</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Deng+Y&amp;cauthor_id=26291195" href="https://pubmed.ncbi.nlm.nih.gov/?term=Deng+Y&amp;cauthor_id=26291195" target="_blank" rel="noopener">Yupu Deng</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Suen+C&amp;cauthor_id=26291195" href="https://pubmed.ncbi.nlm.nih.gov/?term=Suen+C&amp;cauthor_id=26291195" target="_blank" rel="noopener">Colin Suen</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Taha+M&amp;cauthor_id=26291195" href="https://pubmed.ncbi.nlm.nih.gov/?term=Taha+M&amp;cauthor_id=26291195" target="_blank" rel="noopener">Mohamad Taha</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Chaudhary+KR&amp;cauthor_id=26291195" href="https://pubmed.ncbi.nlm.nih.gov/?term=Chaudhary+KR&amp;cauthor_id=26291195" target="_blank" rel="noopener">Ketul R Chaudhary</a>,<a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Courtman+DW&amp;cauthor_id=26291195" href="https://pubmed.ncbi.nlm.nih.gov/?term=Courtman+DW&amp;cauthor_id=26291195" target="_blank" rel="noopener"> David W Courtman</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Stewart+DJ&amp;cauthor_id=26291195" href="https://pubmed.ncbi.nlm.nih.gov/?term=Stewart+DJ&amp;cauthor_id=26291195" target="_blank" rel="noopener">Duncan J Stewart</a>.Affiliations ExpandPMID: 26291195 DOI: <a data-mce-href="https://doi.org/10.1165/rcmb.2014-0488oc" href="https://doi.org/10.1165/rcmb.2014-0488oc" target="_blank" rel="noopener">10.1165</a>/<a data-mce-href="https://doi.org/10.1165/rcmb.2014-0488oc" href="https://doi.org/10.1165/rcmb.2014-0488oc" target="_blank" rel="noopener">rcmb.2014-0488OC</a> Abstract We assessed the pulmonary hemodynamic response to vascular endothelial growth factor receptor, type 2, inhibition using SU5416 (SU) with and without chronic hypoxia (CH) in different background strains and colonies of rats. A single subcutaneous injection of SU (20 mg/kg) or vehicle was administered to different substrains of Sprague-Dawley (SD) rats, and they were compared with Lewis and Fischer rats, with and without exposure to CH (10% O2 for 3 wk). Remarkably, a unique colony of SD rats from Charles River Laboratories, termed the SD-hyperresponsive type, exhibited severe pulmonary arterial hypertension (PAH) with SU alone, characterized by increased right ventricular systolic pressure, right ventricular/left ventricular plus septal weight ratio, and arteriolar occlusive lesions at 7-8 weeks (all P &lt; 0.0001 versus vehicle). In contrast, the other SD substrain from Harlan Laboratories, termed SD-typical type, as well as Fischer rats, developed severe PAH only when exposed to SU and CH, whereas Lewis rats showed only a minimal response. All SD-typical type rats survived for up to 13 weeks after SU/CH, whereas SD-hyperresponsive type rats exhibited mortality after SU and SU/CH (35% and 50%, respectively) at 8 weeks. Fischer rats exposed to SU/CH exhibited the greatest mortality at 8 weeks (78%), beginning as early as 4 weeks after SU and preceded by right ventricle enlargement. Of note, a partial recovery of PAH after 8 weeks was observed in the SD-typical type substrain only. In conclusion, variation in strain, even between colonies of the same strain, has a remarkable influence on the nature and severity of the response to SU, consistent with an important role for genetic modifiers of the PAH phenotype.Keywords: SU5416; pulmonary arterial hypertension; right ventricular remodeling; rodent strains; vascular remodeling.<a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/26291195/" href="https://pubmed.ncbi.nlm.nih.gov/26291195/">Link</a>

Marked Strain-Specific Differences in the SU5416 Rat Model of Severe Pulmonary Arterial Hypertension

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Bosentan does not improve pulmonary hypertension and lung...

Marked Strain-Specific Differences in the SU5416 Rat Mode...