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Abstrakt
Landiolol Hydrochloride Normalizes Diminished Levels of Cardiac Vascular Endothelial Growth Factor (VEGF) Signaling System Components in Lipopolysaccharide-Induced Sepsis Independent of Inflammatory Markers
Yoshimoto Seki, Subrina Jesmin, Majedul Islam, Yoshiyasu Ogura, Masami Oki, Nobutake Shimojo, Tanzila Khatun, Hideaki Sakuramoto, Satoru Kawano and Taro Mizutani
Aim: Myocardial dysfunction is one of the complications associated with sepsis during its (sepsis) pathogenesis. To date, very few studies have investigated whether angiogenic factors in the heart, such as vascular endothelial growth factor (VEGF) and components of its signaling system are involved in myocardial dysfunction during the early phases of sepsis. Therefore, the present study aims to examine: 1) the expression pattern of VEGF and its signaling molecules in the heart during the early hours of LPS-induced sepsis and 2) whether landiolol hydrochloride, an ultrashort-acting beta- blocker, can ameliorate alterations in the expression of cardiac VEGF signaling system components in the rats under these (sepsis) conditions.
Method: Eight (8)-week-old male Wistar rats were administered for three hours with either LPS only once, or continuously with LPS plus landiolol.
Result: At 3 h after LPS (only) administration, circulatory levels of tumor necrosis factor (TNF)-α, IL-6, iNOS, lactate concentration and percentage of fractional shortening of the heart were significantly increased. However, levels of cardiac VEGF and its downstream signaling components were significantly down regulated. Treatment of LPS-administered rats with landiolol for 3 h normalized LPS-induced blood lactate levels, cardiac functional compensatory events, as well as VEGF and its signaling molecules, but did not alter levels of plasma TNF-α, IL-6 and iNOS.
Conclusion: Taken together, these data led us to conclude that landiolol may be cardio-protective in septic rats by normalizing coronary microcirculation through blockage of sepsis-induced decrease in expression of VEGF signaling system but independent of inflammatory cytokines.