Objective:To investigate the effects of levosimendan on renal function in patients with septic cardiomyopathy.Methods:Patients admitted to the Emergency Intensive Care Unit (EICU) of Affiliated Hospital of Nantong University from May 2018 to April 2020 diagnosed with septic cardiomyopathy assessed by pulse-indicator continuous cardiac output (PiCCO) and bedside echocardiograpy and renal ultrasound were retrospectively enrolled and divided into levosimendan group (combined levosimendan with traditional treatment) and control group (traditional treatment). The cardiac index (CI) and other hemodynamic indicators were measured by the PiCCO instrument, the left ventricular ejection fraction (LVEF) and other indicators were measured by bedside echocardiography, and renal blood flow grading and renal resistance index (RRI) were evaluated by bedside renal ultrasound. Changes of hemodynamic indexes and cardiac and renal function at 7 days after treatment were evaluated. The incidence of acute kidney injury (AKI) and the proportion and duration of patients receiving continuous renal replacement therapy (CRRT) for AKI during hospitalization were compared between the two groups, and the clinical outcomes of patients were followed up at 28 days.Results:A total of 56 patients were enrolled, including 25 patients in levosimendan group and other 31 patients in control group. There was no significant difference in baseline characteristics between the two groups (all P>0.05). After 7 days of treatment, compared with the control group, in the levosimendan group, CI was significantly higher [4.5 (3.5, 5.3) L·min -1·m -2 vs. 5.7 (4.6, 7.4) L·min -1·m -2, P=0.004], the LVEF was also significantly higher [40.0 (31.0, 49.0) % vs. 51.0 (39.0, 57.0) % vs, P=0.015], the renal blood flow grading was higher ( P=0.020), and the RRI was significantly lower [0.67 (0.62, 0.74) vs. 0.62 (0.56, 0.69), P=0.034]. There was no significant difference in the proportion of AKI and the proportion of CRRT required between the two groups during hospitalization (all P>0.05); However, the duration of CRRT treatment for AKI in levosimendan group was significantly shorter than that in the control group (56h vs. 73h, P=0.009). There was no significant difference in mortality between levosimendan group and control group at 28 days of follow-up (24.0% vs. 22.6%, P=1.000). Conclusion:In patients with septic cardiomyopathy, levosimendan treatment can improve cardiac function and renal blood flow, and then promote renal function recovery and successful withdrawal of CRRT for those complicating AKI on the treatment of CRRT.

Aim To study the effects of 2 ,3 ,4 ’ ,5-tet-rahydroxystilbene-2-O-β-D glucoside ( TSG ) on myo-cardial fibrosis ( MF) induced by isoproterenol ( ISO) in mice and its possible mechanism. Methods MF in mice was induced by subcutaneous injection of isoprot-erenol for 14 days. TSG (30,60,120 mg·kg-1 ) and captopril ( 40 mg · kg-1 ) were then administered by gavage to mice. The experiment was stopped 12 h after the last administration of the drugs. Hematoxylin-eosin ( HE) and Masson staining were used to estimate the extent of MF. Level of hydroxyproline in myocardial tissues was measured. Protein expressions of collagenⅠ, collagen Ⅲ and transforming growth factor-β1 (TGF-β1) in myocardial tissues were measured. Lev-els of superoxide dismutase ( SOD ) and glutathione peroxidase ( GSH-Px ) were determined. Results Compared with control mice, the level of hydroxypro-line in myocardial tissues was significantly increased in isoproterenol treated mice. Histological sections of iso-proterenol-treated hearts showed extensive myocardial fibrosis. And protein expressions of collagenⅠand col-lagen Ⅲwere markedly increased in isoproterenol trea-ted mice. However, therapy with TSG decreased the level of hydroxyproline in myocardial tissues, ameliora-ted the degree of myocardial fibrosis, and reduced the collagen expressions induced by isoproterenol adminis-tration. Moreover, treatment with TSG decreased TGF-β1 protein expression and elevated the myocardial SOD and GSH-Px activity. Conclusion TSG can inhibit MF formation induced by ISO in mice which might be due to regulating TGF-β1 protein expression and its an-tioxidant effect.