Abstract: TH-PO112
Targeting Oxidative Stress to Prevent Cardiorenal Syndrome in Right Ventricular Failure
Session Information
- AKI: Mechanisms - I
November 02, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Author
- Farahmand, Firoozeh, Saint Louis University, Saint Louis, Missouri, United States
Background
Renal dysfunction remains an independent risk predictor of death and hospitalization in right ventricular failure (RVF) and RV function plays a pivotal role in preventing CRS. However, the pathophysiology of RV failure induced CRS remains poorly understood. The heart and the kidney have complex bidirectional interlinks and there is a growing body of evidence that oxidative stress is a major bidirecional crosstalk mediator of the Heart-kdiney in left ventricualr dusfunction. Clinically driven experimental modeling is crucial to investigate pathophysiology based therapy.
Methods
This study on RVF- Induced CRS investigated changes in antioxidants and oxidative stress in compensated CRS and if antioxidant prevents the pathophysiological heart-kidney cross talk. RVF-Induced CRS in rats was produced by alkaloid (ALK) injection. Rats were treated with antioxidant-LOS, 1 wk. pre & post-ALK injection. At 1 and 2 weeks post-ALK injection, echocardiography was performed to monitor cardiac function. RV systolic pressure (RVSP), RV hypertrophy (RVH), RV function, kidney and RV levels of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSHPx) and lipid peroxidation (LPX). were measured. After sacrificing animals, hearts and kidneys were removed for histopathology and wet /dry weight ratios measurement.
Results
At 1 week, ALK-induced CRS resulted in RVSP, RV hypertrophy and LPX in RV myocardium as well as the kidney. There was a mild increase in antioxidant enzymes activities including SOD and GSHPx in RV and the kidney with no histopathological finding of kidney injury . At 2 weeks post-ALK injection there was RV failure and a significant increase in oxidative stress and antioxidant enzymes in RV and the kidney. Kidney histopathology with Periodic acid-Schiff (PAS) staining demonstrated ATN. Antioxidant-LOS treatment prevents ALK-induced CRS and decreased oxidative in the RV myocardium and the kidney. no change in RV and kidney wet/dry weight ratio between CRS and control animals were obsreved that suggest there was no renal or RV congestion at 2 weeks post ALK-indced CRS.
Conclusion
Since RVF-induced CRS was associated with oxidative stress and antioxidant was able to inhibit these pathophysiological heart-kindey cross talk it is proposed that antixodant modulates cardiac remodelling and ATN in CRS. Therefore, targetting of oxidative stress as an adjunt therapy is suggested.