Metabolic responses in ischemic myocardium after inhalation of carbon monoxide

被引：14

作者：

Ahlstrom, K. ^{[2
]}

Biber, B. ^{[2
]}

Aberg, A. ^{[1
]}

Waldenstrom, A. ^{[1
]}

Ronquist, G. ^{[3
]}

Abrahamsson, P. ^{[1
]}

Stranden, P. ^{[1
]}

Johansson, G. ^{[1
]}

Haney, M. F. ^{[1
]}

机构：

[1] Umea Univ Hosp, S-90185 Umea, Sweden

[2] Sahlgrens Univ Hosp, S-41345 Gothenburg, Sweden

[3] Univ Uppsala Hosp, Clin Chem & Dept Med Sci, Uppsala, Sweden

来源：

ACTA ANAESTHESIOLOGICA SCANDINAVICA | 2009年 / 53卷 / 08期

关键词：

CO-RELEASING MOLECULE; CARDIOPULMONARY BYPASS; HEME OXYGENASE; REPERFUSION INJURY; INFARCT SIZE; IN-VIVO; PROTECTS; HEART; MODEL; PIGS;

D O I：

10.1111/j.1399-6576.2009.01992.x

中图分类号：

R614 [麻醉学];

学科分类号：

100217 ;

摘要：

Background To clarify the mechanisms of carbon monoxide (CO) tissue-protective effects, we studied energy metabolism in an animal model of acute coronary occlusion and pre-treatment with CO. Methods In anesthetized pigs, a coronary snare and microdialysis probes were placed. CO (carboxyhemoglobin 5%) was inhaled for 200 min in test animals, followed by 40 min of coronary occlusion. Microdialysate was analyzed for lactate and glucose, and myocardial tissue samples were analyzed for adenosine tri-phosphate, adenosine di-phosphate, and adenosine mono-phosphate. Results Lactate during coronary occlusion was approximately half as high in CO pre-treated animals and glucose levels decreased to a much lesser degree during ischemia. Energy charge was no different between groups. Conclusions CO in the low-doses tested in this model results in a more favorable energy metabolic condition in that glycolysis is decreased in spite of maintained energy charge. Further work is warranted to clarify the possible mechanistic role of energy metabolism for CO protection.

引用

页码：1036 / 1042

页数：7

共 26 条

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