• Yoshimoto Seki, Subrina Jesmin, Nobutake Shimojo, Md Majedul Islam, Md Arifur Rahman, Tanzila Khatun, Hideaki Sakuramoto, Masami Oki, Aiko Sonobe, Junko Kamiyama, Keiichi Hagiya, Satoru Kawano, and Taro Mizutani.
• Department of Emergency and Critical Care Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
• Life Sci. 2014 Nov 24; 118 (2): 357-63.

AimsLandiolol hydrochloride, an ultra-short-acting highly cardio-selective β-1 blocker, has become useful for various medical problems. Recent studies have demonstrated that co-treatment with landiolol protects against acute lung injury and cardiac dysfunction in rats of lipopolysaccharide (LPS)-induced systemic inflammation, and was also associated with a significant reduction in serum levels of the inflammation mediator HMGB-1 and histological lung damage. Endothelin (ET)-1, a potent vasoconstrictor, has been implicated in pathogenesis of sepsis and sepsis-induced multiple organ dysfunction syndrome. Here, we investigated whether landiolol hydrochloride can play important roles in ameliorating LPS-induced alterations in cardiac ET system of septic rats.Main MethodsEight-week-old male Wistar rats were administered LPS only for 3 h and the rest were treated with LPS as well as with landiolol non-stop for 3 h.Key FindingsAt 3 h after LPS (only) administration, circulatory tumor necrosis factor (TNF)-α level, blood lactate concentration and percentage of fractional shortening of heart were significantly increased. In addition, LPS induced a significant expression of various components of cardiac ET-1 system compared to control. Finally, treatment of LPS-administered rats with landiolol for 3 h normalized LPS-induced blood lactate levels and cardiac functional compensatory events, without altering levels of plasma TNF-α and ET-1. Most strikingly, landiolol treatment significantly normalized various components of cardiac ET-1 signaling system in septic rat.SignificanceTaken together, these data led us to conclude that landiolol may be cardio-protective in septic rats by normalizing the expression of cardiac vasoactive peptide such as ET, without altering the circulatory levels of inflammatory cytokines.Copyright © 2014 Elsevier Inc. All rights reserved.

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