Effects of transverse aortic constriction-induced left ventricular dysfunction on pulmonary vascular remodeling in rats and its relationship with bone morphogenetic protein 7

Autor: HU Junhao, WU Xiaojing, GU Wenzhu, JIN Peng, LIU Jialing, ZHOU Qi
Jazyk: čínština
Rok vydání: 2020
Předmět:
Zdroj: Di-san junyi daxue xuebao, Vol 42, Iss 14, Pp 1385-1391 (2020)
Druh dokumentu: article
ISSN: 1000-5404
DOI: 10.16016/j.1000-5404.202002118
Popis: Objective To study the effects of left ventricular dysfunction induced by transverse aortic constriction (TAC) on pulmonary vascular remodeling and hemodynamics, and the relationship with bone morphogenetic protein 7 (BMP7) expression in the lung tissues of rats. Methods Sixteen healthy male Sprague-Dawley rats were randomized equally into TAC model group and sham operation group. At the end of 9 weeks after the surgery, cardiac remodeling and the changes of cardiac functions were assessed by cardiac ultrasound. The pulmonary hemodynamic parameters and the right ventricular functions were evaluated by cardiac catheterization. HE and Masson staining was used to observe pulmonary vascular remodeling, left ventricular myocardial cell size and left ventricular myocardial cell fibrosis in the rats. The mRNA and protein levels of BMP7 in the lung tissues of the rats were detected using RT-qPCR and Western blotting. Results Compared with the sham-operated rats, the rats with TAC showed significantly increased left ventricular wall and septal thickness, increased left ventricular end-diastolic volume (P < 0.01), and decreased left ventricular ejection fraction (P < 0.01). Hemodynamic analysis showed significant increases of the mean pulmonary arterial pressure (mPAP) and right ventricular systolic pressure (RVSP) in rats with TAC as compared with the sham-operated rats (P < 0.01). Pathological examination revealed that in rats with TAC, the cross-sectional area of the left ventricular cardiomyocytes increased significantly (P < 0.01) with obvious myocardial fibrosis (P < 0.01) and thickening of the medial layer of the pulmonary arterioles (P < 0.01) in comparison with the sham-operated group. The expression of BMP7 was decreased significantly at both the mRNA and protein levels in the pulmonary tissue in TAC group as compared with the sham-operated group (P < 0.05). Conclusion Pulmonary hypertension and pulmonary vascular remodeling caused by left ventricular remodeling and left ventricular dysfunction might be related to decreased pulmonary BMP7 expression in addition to the direct influence by changes in the hemodynamics, suggesting that the organ crosstalk between the heart and the lung might participate in the occurrence of pulmonary hypertension resulting from left heart diseases.
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