title: Distinct right ventricle remodeling in response to pressure overload in the rat.
abstract: Pulmonary arterial hypertension (PAH), the most serious chronic disorder of the pulmonary circulation, is characterized by pulmonary vasoconstriction and remodeling, resulting in increased afterload on the right ventricle (RV). In fact, RV function is the main determinant of prognosis in PAH. The most frequently used experimental models of PAH include monocrotaline- and chronic hypoxia-induced PAH, which primarily affect the pulmonary circulation. Alternatively, pulmonary artery banding (PAB) can be performed to achieve RV overload without affecting the pulmonary vasculature, allowing researchers to determine the RV-specific effects of their drugs/interventions. In this work, using two different degrees of pulmonary artery constriction, we characterize, in full detail, PAB-induced adaptive and maladaptive remodeling of the RV at 3 wk after PAB surgery. Our results show that application of a mild constriction resulted in adaptive hypertrophy of the RV, with preserved systolic and diastolic function, while application of a severe constriction resulted in maladaptive hypertrophy, with chamber dilation and systolic and diastolic dysfunction up to the isolated cardiomyocyte level. By applying two different degrees of constriction, we describe, for the first time, a reliable and short-duration PAB model in which RV adaptation can be distinguished at 3 wk after surgery. We characterize, in full detail, structural and functional changes of the RV in its response to moderate and severe constriction, allowing researchers to better study RV physiology and transition to dysfunction and failure, as well as to determine the effects of new therapies.
authors.affiliation: Deparment of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal; and.
authors.forename: P
authors.initials: P
authors.lastname: Mendes-Ferreira
authors.affiliation: Deparment of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal; and.
authors.forename: D
authors.initials: D
authors.lastname: Santos-Ribeiro
authors.affiliation: Deparment of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal; and.
authors.forename: R
authors.initials: R
authors.lastname: Adão
authors.affiliation: Deparment of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal; and.
authors.forename: C
authors.initials: C
authors.lastname: Maia-Rocha
authors.affiliation: Deparment of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal; and.
authors.forename: M
authors.initials: M
authors.lastname: Mendes-Ferreira
authors.affiliation: Deparment of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal; and.
authors.forename: C
authors.initials: C
authors.lastname: Sousa-Mendes
authors.affiliation: Deparment of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal; and.
authors.forename: A F
authors.initials: AF
authors.lastname: Leite-Moreira
authors.affiliation: Deparment of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal; and Faculty of Nutrition and Food Sciences, University of Porto, Porto, Portugal carmensb@med.up.pt.
authors.forename: C
authors.initials: C
authors.lastname: Brás-Silva
mesh_terms: D000223:Adaptation, Psychological; D000818:Animals; D062186:Arterial Pressure; D020013:Calcium Signaling; D003250:Constriction; D004195:Disease Models, Animal; D005355:Fibrosis; D006976:Hypertension, Pulmonary / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D017380:Hypertrophy, Right Ventricular / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D011651:Pulmonary Artery / Q000503:physiopathology* / Q000601:surgery; D017208:Rats, Wistar; D013997:Time Factors; D018497:Ventricular Dysfunction, Right / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right; D020257:Ventricular Remodeling
keywords: pulmonary artery banding; pulmonary hypertension; right ventricle remodeling