Depletion of myocardial glucose is observed during endotoxemic but not hemorrhagic shock in a porcine model
Depletion of myocardial glucose is observed during endotoxemic but not hemorrhagic shock in a porcine model
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DOI：
10.1186/cc12843
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发表时间：
2013-01-01
期刊：
影响因子：
15.1
通讯作者：
Barnett, Adrian G.
中科院分区：
文献类型：
--
作者：
Chew, Michelle S.;Shekar, Kiran;Barnett, Adrian G.
前言代谢功能障碍是脓毒症的特征之一，但对心脏等关键器官的局部变化知之甚少。本研究的目的是通过使用微透析(MD)直接测量葡萄糖、乳酸和丙酮酸等底物来比较在体猪内毒素血症和失血性休克时心肌代谢的变化。方法26头母猪随机分为对照组(C组，n=8)、内毒素休克组(E组，n=9)和失血性休克组(H组，n=9)。结果E组心肌血糖较对照组明显降低，而H组与对照组比较差异无统计学意义(C/L均值差：C与E-1.5(-2.2~-0.8)，P=0.001；H与E-1.1(-1.8~-0.4)，P=0.004；C与H-0.4(-1.1~0.3)，P=0.282)。两个休克组的心肌丙酮酸增加了四倍，乳酸增加了三倍，两种类型的休克之间没有差别。没有证据表明心肌无氧代谢，所有动物的乳酸：丙酮酸(L：P)比率正常，无论休克类型。在骨骼肌中，只有E组观察到葡萄糖浓度下降(平均差值：C比E-0.8(-1.4%至-0.3%，P=0.007)。虽然两个休克组的骨骼肌乳酸均升高，但仅E组伴有丙酮酸升高(平均差值：C与E121(46~195)，P=0.003；H与E77(7~147)，P=0.032；C与H43(-30~43)，P=0.229)。失血性休克后，骨骼肌组织中L与P的比值升高，而内毒素血症无明显变化。结论内毒素血症可引起心肌葡萄糖水平的快速下降，而不是出血。尽管血糖降低，但心肌乳酸和丙酮酸浓度升高，与失血性休克时没有什么不同。在骨骼肌中，内毒素休克时的底物模式类似于心肌中的底物模式。失血性休克时，骨骼肌反应的特点是丙酮酸缺乏增加，L：P比值升高。因此，内毒素休克时心肌的代谢模式与失血性休克时不同。骨骼肌和心肌在内毒素休克时表现出相似的底物模式，但在失血性休克时有所不同。
IntroductionMetabolic dysfunction is one of the hallmarks of sepsis yet little is known about local changes in key organs such as the heart. The aim of this study was to compare myocardial metabolic changes by direct measurements of substrates, such as glucose, lactate and pyruvate, using microdialysis (MD) in in-vivo porcine endotoxemic and hemorrhagic shock. To assess whether these changes were specific to the heart, we simultaneously investigated substrate levels in skeletal muscle.MethodsTwenty-six female pigs were randomized to three groups: control (C) n = 8, endotoxemic shock (E) n = 9 and hemorrhagic shock (H) n = 9. Interstitial myocardial pyruvate, lactate and glucose were measured using MD. Skeletal muscle MD was also performed in all three groups.ResultsMarked decreases in myocardial glucose were observed in the E group but not in the H group compared to controls (mean difference (CI) in mmol/L: C versus E -1.5(-2.2 to -0.8), P < 0.001; H versus E -1.1(-1.8 to -0.4), P = 0.004; C versus H -0.4(-1.1 to 0.3), P = 0.282). Up to four-fold increases in myocardial pyruvate and three-fold increases in lactate were seen in both shock groups with no differences between the two types of shock. There was no evidence of myocardial anaerobic metabolism, with normal lactate: pyruvate (L:P) ratios seen in all animals regardless of the type of shock.In skeletal muscle, decreases in glucose concentrations were observed in the E group only (mean difference: C versus E -0.8(-1.4 to -0.3), P = 0.007). Although skeletal muscle lactate increased in both shock groups, this was accompanied by increases in pyruvate in the E group only (mean difference: C versus E 121(46 to 195), P = 0.003; H versus E 77(7 to 147), P = 0.032; C versus H 43(-30 to 43), P = 0.229). The L:P ratio was increased in skeletal muscle in response to hemorrhagic, but not endotoxemic, shock.ConclusionsEndotoxemia, but not hemorrhage, induces a rapid decrease of myocardial glucose levels. Despite the decrease in glucose, myocardial lactate and pyruvate concentrations were elevated and not different than in hemorrhagic shock. In skeletal muscle, substrate patterns during endotoxemic shock mimicked those seen in myocardium. During hemorrhagic shock the skeletal muscle response was characterized by a lack of increase in pyruvate and higher L: P ratios. Hence, metabolic patterns in the myocardium during endotoxemic shock are different than those seen during hemorrhagic shock. Skeletal muscle and myocardium displayed similar substrate patterns during endotoxemic shock but differed during hemorrhagic shock.