Hydralazine Attenuates Lipopolysaccharide-Induced Murine Myocardial Dysfunction by Inhibition of Semicarbazide-Sensitive Amine Oxidase.

ABSTRACT: Sepsis-induced myocardial dysfunction (SIMD) is a fatal complication with limited therapeutic options. Semicarbazide-sensitive amine oxidase (SSAO) contributes to oxidative stress and leukocyte recruitment, yet its role in SIMD remains unexplored. This study investigates whether hydralazine, a potent SSAO inhibitor, protects against SIMD by evaluating the involvement of SSAO inhibition. Using a murine model of LPS-induced sepsis, hydralazine was administered 30 min post-injection. Over a 7-day observation period, survival rates, cardiac function (assessed by echocardiography), and myocardial injury (evaluated via plasma biomarkers including CK, CK-MB, LDH, and AST, alongside histopathology) were monitored. Additional analyses included measurements of oxidative stress markers (T-AOC, GSH-PX

SUBMITTER: Kuang Z 

PROVIDER: S-EPMC12729300 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature