Exploring Beta Blockers’ Efficacy in Sepsis-Induced Acute Lung Injury and HMGB1-sRAGE Interaction

Background and Objective: Beta-blockers improve cardiac function and prevent catecholamine-mediated hypermetabolism in critically ill patients.This study investigated the role of beta blockers in reducing inflammation in a sepsis model and their influence on acute lung injury (ALI).The study aimed to understand beta blockers' potential role in mitigating ALI risk in sepsis patients.Materials and Methods: Fifty Wistar albino rats were divided into five groups.The first group was the control and the remaining four had feces-induced peritonitis (FIP) to mimic sepsis.The second group was the FIP group, while the third, fourth and fifth groups received different intraperitoneal doses of beta-blockers: 10 mg/kg/day of propranolol, 2 mg/kg/day of metoprolol and 5 mg/kg/day of carvedilol.Results: Beta-blocker administration in FIP rats significantly decreased inflammatory biomarkers, including Tumor Necrosis Factor-alpha (TNF-"), lactic acid, Interleukin-6 (IL-6), malondialdehyde (MDA), high mobility group box 1 (HMGB1) and Interleukin-1 beta (IL-1$), compared to the FIP+Saline group.The FIP+beta blockers group exhibited elevated Soluble Receptors for Advanced Glycation End product (s-RAGE) levels compared to the FIP+saline group.Carvedilol, metoprolol and propranolol showed distinct mechanisms, resulting in biochemical improvements in sepsis and curative effects observed in computed tomography and histology.These findings suggested that beta-blockers may effectively prevent ALI side effects in sepsis treatments.Conclusion: Commencing beta-blocker treatment alongside standard sepsis therapy could potentially protect against adverse effects like ALI.It is recommended to consider adding beta-blockers to standard sepsis treatment regimens.