Additional file 1: Table S1. of Investigation of the pathophysiology of cardiopulmonary bypass using rodent extracorporeal life support model

Ion variable measurements before and after ECLS. (DOCX 64 kb

Hyperleptinemia positively associated with central arterial stiffness in hemodialysis patients

<div><p>Objective</p><p>Leptin plays a role in stimulating vascular inflammation, vascular smooth muscle hypertrophy, and augmenting blood pressure, which contributes to the pathogenesis of atherosclerosis and leads to arterial stiffness. This vascular damage, measured by carotid-femoral pulse wave velocity (cfPWV), is recognized as an independent predictor of cardiovascular mortality in hemodialysis (HD) patients. The aim of this study was to evaluate the relationship between serum leptin and arterial stiffness in HD patients.</p><p>Patients and methods</p><p>In 112 of the 126 HD patients were eligible and their biochemical data were collected for analysis. Serum leptin level was measured using a commercial enzyme-linked immunosorbent assay kit. Carotid-femoral pulse wave velocity was measured by a validated tonometry system (SphygmoCor). Those have cfPWV values above 10 m/s are defined as the high arterial stiffness group.</p><p>Results</p><p>Among the participants, thirty-eight of them who were in the high arterial stiffness group, had a higher prevalence of diabetes mellitus (p = 0.002), age (p = 0.029), body mass index (BMI, p = 0.018), body fat mass (p = 0.001), hemoglobin (p = 0.040), and serum leptin levels (P<0.001). Multivariable logistic regression analysis showed that leptin (odds ratio [OR] 1.09; 95% confidence interval [CI] 1.04–1.14; p <0.001), diabetes (OR 7.17; CI 1.39–37.00; p = 0.019), body fat mass (OR 1.16; CI 1.02–1.33; p = 0.027); and hemoglobin (OR 2.11; CI 1.15–3.87; p = 0.015) were independently associated with arterial stiffness in HD patients.</p><p>Conclusion</p><p>In our study, hyperleptinemia was positively correlated to the high cfPWV and thus was related to high arterial stiffness in HD patients.</p></div

Distribution of hemodialysis patients with high or low arterial stiffness in subgroup analysis.

<p>Distribution of hemodialysis patients with high or low arterial stiffness in subgroup analysis.</p

Clinical characteristics and serum leptin levels of 112 hemodialysis patients.

<p>Clinical characteristics and serum leptin levels of 112 hemodialysis patients.</p

Clinical variables of the 112 hemodialysis patients with high or low arterial stiffness.

<p>Clinical variables of the 112 hemodialysis patients with high or low arterial stiffness.</p

Correlation between serum leptin levels and clinical variables among 112 hemodialysis patients.

<p>Correlation between serum leptin levels and clinical variables among 112 hemodialysis patients.</p

Study design.

<p>Study design.</p

Effects of either ALC or OXF on cardiac levels of MDA/TBARS in DM.

<p>NC, normal controls; NC+ALC, NC treated with ALC; NC+OXF, NC treated with OXF; DM, STZ-induced diabetic rats; DM+ALC, DM treated with ALC; DM+OXF, DM treated with OXF; ALC, acetyl-L-carnitine; OXF, oxfenicine.</p

Effects of either ALC or OXF on <i>P_iso</i>_max (A), <i>V_eed</i> (B), and <i>E</i>_max (C) in DM. <i>E</i>_max can be determined by the ratio of <i>P_iso</i>_max to <i>V_eed</i>.

<p>NC, normal controls; NC+ALC, NC treated with ALC; NC+OXF, NC treated with OXF; DM, STZ-induced diabetic rats; DM+ALC, DM treated with ALC; DM+OXF, DM treated with OXF; ALC, acetyl-L-carnitine; OXF, oxfenicine; <i>P_iso</i>_max, the estimated peak isovolumic pressure; <i>V_eed</i>, the effective LV end-diastolic volume; <i>E</i>_max, the maximal systolic elastance.</p

Effects of either ALC or OXF on hemodynamic parameters in the STZ-diabetic rats.

<p>All values are expressed as means ± SE. <i>HR</i>, basal heart rate (beats min⁻¹); <i>CO</i>, cardiac output (mL s⁻¹); <i>CI</i>, cardiac index (L min⁻¹ m⁻²); <i>MAP</i>, mean aortic pressure (mmHg). NC, normal controls; NC+ALC, NC treated with ALC; NC+OXF, NC treated with OXF; DM, STZ-diabetic rats; DM+ALC, DM treated with ALC; DM+OXF, DM treated with OXF; ALC, acetyl-L-carnitine; OXF, oxfenicine.</p>†<p>Statistical difference (<i>P</i><0.05) from the NC.</p>‡<p>Statistical difference (<i>P</i><0.05) from the DM.</p