Premium
Metabolic responses in ischemic myocardium after inhalation of carbon monoxide
Author(s) -
AHLSTRÖM K.,
BIBER B.,
ÅBERG A.,
WALDENSTRÖM A.,
RONQUIST G.,
ABRAHAMSSON P.,
STRANDÉN P.,
JOHANSSON G.,
HANEY M. F.
Publication year - 2009
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.2009.01992.x
Subject(s) - medicine , microdialysis , coronary occlusion , adenosine , carboxyhemoglobin , ischemia , energy charge , anesthesia , glycolysis , carbon monoxide , energy metabolism , ischemic preconditioning , cardiology , high energy phosphate , metabolism , biochemistry , phosphocreatine , chemistry , receptor , adenylate kinase , catalysis , central nervous system
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.