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• W1985149751 abstract "Septic shock decreases cardiac hydraulic work relative to the rate of myocardial oxygen consumption, causing decreased mechanical efficiency (hydraulic work/myocardial oxygen consumption). This study tested whether the mitochondrial uncoupling protein UCP2 was responsible for decreased cardiac mechanical efficiency after polymicrobial septic shock. Sepsis was initiated in ketamine/xylazine-anesthetized rats by cecal ligation and puncture (CLP). Steady-state mRNA content was quantified by Northern blot analysis, and protein content was estimated by western blot. Additional hearts were removed after 12 h and perfused in working mode to measure work (mmHg x mL/min/100g dry wt) and efficiency (CE= work/ oxygen consumption, %). The 72-h mortality rate was 80%, and deaths occurred between 12–32 h. Cardiac work (152 ± 15, shock vs. 235 ± 16, control;P < 0.05) and cardiac efficiency (4.0 ± 0.4 vs. 5.6 ± 0.3;P < 0.05) were significantly decreased when hearts were isolated 12 h after CLP. Myocardial UCP2 mRNA expression was increased by 52% (12 h) compared with control hearts; however, there was no detectable UCP2 protein in mitochondria isolated from either control or septic hearts. Conclusions: Although polymicrobial sepsis decreased cardiac mechanical efficiency and increased UCP-2 expression coincident with premortal hypothermia, we did not detect any evidence of UCP-2 protein in septic heart muscle. These data argue against the hypothesis that UCP-2 causes decreased cardiac mechanical efficiency in septic shock." @default.
• W1985149751 created "2016-06-24" @default.
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• W1985149751 date "2003-06-01" @default.
• W1985149751 modified "2023-10-14" @default.
• W1985149751 title "Cardiac UCP2 Expression and Myocardial Oxidative Metabolism During Acute Septic Shock in the Rat" @default.
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• W1985149751 doi "https://doi.org/10.1097/01.shk.0000055241.25446.5f" @default.
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