Relationship of PCr with pO₂.

<p>Relationship of PCr with pO₂.</p

Deoxymyoglobin Data.

<p>Values are means ± SE. * P<0.05 vs. Baseline.</p><p>Deoxymyoglobin Data.</p

Relationship of ATP with pO₂.

<p>Relationship of ATP with pO₂.</p

Myocardial blood flow, oxygen consumption, and arterial - venous blood gas data.

<p>Values are Mean±SD, * p<0.05 vs. Baseline.</p><p>Myocardial blood flow, oxygen consumption, and arterial - venous blood gas data.</p

Relationship of Myocardial Blood Flow and Tissue Oxygenation with Oxygen Fraction of Inspired Gas.

<p>DMB  =  level of deoxymyoglobin normalized to total LAD occlusion; MBF  =  myocardial blood flow rate (ml per minute per gram myocardium measured by microspheres at each experimental conditions). *, p<0.01 VS Baseline; #, p<0.01 VS. LAD occlusion.</p

Hemodynamic Data.

<p>Values are means ± SD. * P<0.05 vs Baseline.</p><p>Hemodynamic Data.</p

Myocardial PCr/ATP and Pi/PCr Data.

<p>Values are means ± SE. * P<0.05 vs. Baseline. † P<0.01 vs. Baseline.</p><p>Myocardial PCr/ATP and Pi/PCr Data.</p

Rotenone induced inflammatory cytokine expression in BV2 cells.

<p>(A) BV2 cells were treated with different doses of rotenone or LPS for 24 hours. The TNFα levels in the cultured media were measured using ELISA assays. The data are presented as the mean ± S.E.M. n = 3, **p<0.01, one-way ANOVA. (B) Immunoblot analysis to detect iNOS expression in the BV2 cells treated with rotenone or LPS. (C) Quantitative analysis of the data from (B), showing the density of iNOS relative to that of the loading control (tubulin). The data are presented as the mean ± S.E.M. n = 3, **p<0.01, ***p<0.001, one-way ANOVA.</p

Rotenone induced microglial activation via p38 MAPK.

<p>(A) BV2 cells were treated with different doses of rotenone for 6 hours or 1 µg/mL LPS for 1 hour and lysed in lysis buffer. The lysates were immunoblotted with the indicated antibodies. (B) Quantitative analysis of the data from (A), showing the density of pp38 relative to that of the loading control (tubulin). The data are presented as the mean ± S.E.M. n = 3, *p<0.05, one-way ANOVA. (C) BV2 cells were treated with 1 µM rotenone for 6 hours or 1 µg/mL LPS for 1 hour or co-treated with 5 mM NAC and either 1 µM rotenone for 6 hours or 1 µg/mL LPS for 1 hour. The cells were stained with an ROS indicator, DCFH-DA, for 30 minutes. The scale bar represents 10 µm. (D) BV2 cells were treated with rotenone or LPS in the same manner described in (C). The cells were lysed, and the lysates were immunoblotted with the indicated antibodies.</p

NAC blocked the rotenone-induced microglial activation.

<p>(A) BV2 cells treated with 1 µM rotenone for 24 hours or 1 µg/mL LPS for 24 hours or co-treated with 5 mM NAC and either 1 µM rotenone for 24 hours or 1 µg/mL LPS for 24 hours. The TNFα levels in the culture media of the treated BV2 cells were measured by ELISA. (B) BV2 cells were treated with as indicated in (A). Then, the cells were lysed, and the lysates were immunoblotted with the indicated antibodies. The activated IL-1β cleaved by caspase-1 is indicated as cleaved IL-1β.</p