22 research outputs found
Effects of LPS and MP on basal heart rate (<i>HR</i> in A), mean aortic pressure (<i>P<sub>m</sub></i> in B), cardiac output (<i>CO</i> in C) and total peripheral resistance (<i>R<sub>p</sub></i> in D).
<p>Data are expressed as mean±s.e. LPS, lipopolysaccharide; MP, methylprednisolone. (<i>n</i> = 10 in each group).</p
Effects of LPS and MP on the plasma levels of NO (Nitrites+Nitrates) (A), Peroxynitrite (nitrotyrosin) (B), CRP (C), and IL-6 (D).
<p>Data are expressed as mean±s.e. LPS, lipopolysaccharide; MP, methylprednisolone; NO, nitric oxide; CRP, C-reactive protein; IL-6, interleukin-6. (<i>n</i> = 10 in each group).</p
Effects of LPS and MP on aortic characteristic impedance (<i>Z<sub>c</sub></i> in A), systemic arterial compliance at mean aortic pressure (<i>C<sub>m</sub></i> in B), wave reflection factor (<i>R<sub>f</sub></i> in C) and wave transit time (<i>Ï„</i> in D).
<p>Data are expressed as mean±s.e. LPS, lipopolysaccharide; MP, methylprednisolone. (<i>n</i> = 10 in each group).</p
Body weight (BW, g), left ventricular weight (LVW, g), ratio of the LVW to BW (LVW/BW, mg/g), and rectal temperature (RT, °C) in the animals.
<p>All values are expressed as mean±s.e. LPS-MP, LPS rats treated with MP; LPS, lipopolysaccharide; MP, methylprednisolone.</p>†<p><i>p</i><0.05 from the Sham group;</p>‡<p><i>p</i><0.05 from the LPS group.</p
Effects of LPS and MP on the expression of AGEs (A), RAGE (B), and iNOS (C) in the aortas.
<p>AGEs and RAGE expressions were probed using immunohistochemical staining (400x). The arrows indicated the sites of antibody staining. iNOS expression (red color) was explored using immunocytochemical fluorescence staining (200x). LPS, lipopolysaccharide; MP, methylprednisolone; AGEs, advanced glycation end products; RAGE, receptor for AGEs; iNOS, inducible nitric oxide synthase.</p
Effects of LPS and MP on aortic AGEs, RAGE, and iNOS proteins measured by Western blotting technique.
<p>Protein expression was normalized to β-actin. Data are expressed as mean±s.e. LPS, lipopolysaccharide; MP, methylprednisolone; LM, LPS groups treated with MP; iNOS, inducible nitric oxide synthase; AGEs, advanced glycation end products; RAGE, receptor for AGEs. (<i>n</i> = 10 in each group).</p
Effects of ALC and of OXF on blood glucose level, body weight, and left ventricular weight in the STZ-diabetic rats.
<p>All values are expressed as means ± SE. BS, blood sugar (mg dL<sup>−1</sup>); BW, body weight (g); LVW, left ventricular weight (g); LVW/BW, ratio of the LVW to BW (mg g<sup>−1</sup>). 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
The solid lines of A and B show the measured ascending aortic flow signal and the LV pressure waveform, respectively, of one control rat.
<p>In Graph B, the dashed line represents the isovolumic pressure curve at an end-diastolic volume, which is estimated by fitting a sinusoidal function to the isovolumic portions of the measured LV pressure. Graphs C and D show the measured data and model-generated data when the elastance-resistance model is fit over <i>t<sub>ej</sub></i><<i>t</i><<i>t<sub>piso</sub></i><sub>max</sub>; <i>t<sub>ej</sub></i> is the onset of ventricular ejection and <i>t<sub>piso</sub></i><sub>max</sub> is the time of peak isovolumic pressure. In Graph C, the solid line represents measured data, and dashed lines represent model-derived data. In Graph D, the dashed line has the slope of regression that equals 1.0. The solid line represents the relation between the measured and model-generated data. <i>P</i>(<i>t</i>) is the measured LV pressure; <i>P<sub>iso</sub></i>(<i>t</i>) is the estimated isovolumic pressure; <i>P</i>(<i>t</i>)/<i>P<sub>iso</sub></i>(<i>t</i>) is the ratio of <i>P</i>(<i>t</i>) to <i>P<sub>iso</sub></i>(<i>t</i>).</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 hemodynamic parameters in the STZ-diabetic rats.
<p>All values are expressed as means ± SE. <i>HR</i>, basal heart rate (beats min<sup>−1</sup>); <i>CO</i>, cardiac output (mL s<sup>−1</sup>); <i>CI</i>, cardiac index (L min<sup>−1</sup> m<sup>−2</sup>); <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