Volume Load-Induced Right Ventricular Failure in Rats Is Not Associated With Myocardial Fibrosis
Myocardial fibrosis
Volume overload
Peripheral edema
DOI:
10.3389/fphys.2021.557514
Publication Date:
2021-02-26T05:36:28Z
AUTHORS (10)
ABSTRACT
Right ventricular (RV) function and failure are key determinants of morbidity mortality in various cardiovascular diseases. Myocardial fibrosis is regarded as a contributing factor to heart failure, but its importance RV has been challenged. This study aims assess whether myocardial drives the transition from compensated decompensated volume load-induced dysfunction.Wistar rats were subjected aorto-caval shunt (ACS, n = 23) or sham (control, 15) surgery, sacrificed after 1 month, 3 months, 6 months. Echocardiography, pressure-volume analysis, assessment gene expression cardiac histology performed.At 6/8 ACS-rats (75%) showed clinical signs (pleural effusion, ascites and/or liver edema), whereas at month no had developed yet. Cardiac output increased two- threefold biventricular dilatation occurred, while LV ejection fraction gradually decreased. At end-systolic elastance (Ees) remained unaltered, Ees decreased substantially. In RV, oxidative stress, inflammation, pro-fibrotic signaling (TGFβ1 pSMAD2/3), present any time point.In ACS rat model, long-term load was initially well tolerated induced overt end-stage However, developed. These findings indicate that not involved dysfunction this model.
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