Addition of α-Ketoglutarate to Blood Cardioplegia Improves Cardioprotection

Kjellman, Ulf; Björk, Kerstin; Ekroth, Rolf; Karlsson, Hans; Jagenburg, Rudolf; Nilsson, Folke; Svensson, Gunnar; Wernerman, Jan

doi:10.1016/s0003-4975(97)00213-0

Cited by 36 publications

(20 citation statements)

References 17 publications

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“…These data are consistent with other reports indicating that α-ketoglutarate prevents ischemic injury [44,45]. Kjellman et al have argued that improved myocardial protection is the result of provision of α-ketoglutarate, which may preserve cell metabolic state [45]. A low myocardial content of α-ketoglutarate during heart surgery might aggravate ischemic injury [44].…”

Section: Discussionsupporting

confidence: 91%

“…It is supposed that the influence of α-ketoglutarate on energy metabolism is realized by cholinesterase inhibition and increase of acetylcholine content [43]. These data are consistent with other reports indicating that α-ketoglutarate prevents ischemic injury [44,45]. Kjellman et al have argued that improved myocardial protection is the result of provision of α-ketoglutarate, which may preserve cell metabolic state [45].…”

Section: Discussionsupporting

confidence: 84%

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Protective role of pinacidil against adrenaline-induced myocardium injury in guinea pig liver mitochondria

Tkachenko

Kurhalyuk²

2007

Open Life Sciences

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Abstract:We investigated the role of the ATP-sensitive potassium channel opener pinacidil and blocker glibenclamide on guinea pig liver mitochondrial function, and a possible significance of pinacidil in the pharmacological treatment during myocardium dystrophy. First, a series of experiments was performed to determine the effect of pinacidil and glibenclamide on mitochondrial oxygen consumption. We found that pinacidil increased the rate of mitochondrial respiration for FAD-generated substrate (succinate oxidation), but was most effective for α-ketoglutarate oxidation with enhancement of respiratory control ratio. Oxidation of FAD-generated substrate inhibited efficiency of phosphorylation for α-ketoglutarate oxidation in pinacidil-treated animals. Glibenclamide decreased the rate of respiration with the lowest value of efficiency of phosphorylation, especially for α-ketoglutarate oxidation. A second series of experiments was performed to determine the effects of pinacidil and glibenclamide on oxidative phosphorylation during adrenaline-induced myocardium dystrophy. The increase in respiratory control ratio and efficiency of phosphorylation for α-ketoglutarate oxidation was greater than for succinate oxidation in mitochondria of pinacidil-pretreated animals during myocardium dystrophy. Inhibitory analysis with malonate suggested that endogenous succinate increased oxidation of NADH-generated substrates in mitochondria. Pinacidil is mainly involved in the adrenaline-induced alterations of mitochondrial function due to elevation of phosphorylation efficiency for α-ketoglutarate oxidation and a decreased level of lipid peroxidation.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 84%

Protective role of pinacidil against adrenaline-induced myocardium injury in guinea pig liver mitochondria

Tkachenko

Kurhalyuk²

2007

Open Life Sciences

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“…Studies using animal models have shown that dietary supplementation with AKG has favorable effects on energy status, protein synthesis, growth, and performance (Junghans et al, 2006;Hou et al, 2011;Dobrowolski et al, 2013;Yao et al, 2012) and can potentially prevent the development of several systemic diseases commonly found in the elderly (Kjellman et al, 1997;Harisson and Pierzhynowski, 2008;Niemiec et al, 2011;Radzki et al, 2012). Protective properties of AKG were also demonstrated in hyperammonemia, hyperaminoaciduria, or exposures to toxic nitrogen chemicals such as cyanide, ammonia, ammonium compounds, amines and hydrazines (Bhattacharya et al, 2002;Dakshayani et al, 2006;Bhattacharya et al, 2009).…”

Section: Alpha-ketoglutarate (Akg) Is An Important Intermediate In Thmentioning

confidence: 99%

Alpha-ketoglutarate attenuates toxic effects of sodium nitroprusside and hydrogen peroxide in Drosophila melanogaster

Bayliak

Shmihel

Lylyk

et al. 2015

Environmental Toxicology and Pharmacology

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“…Accordingly, the addition of glucose and/or lactate to cardioplegic solutions has no convincing cardioprotective effect (2,11,33,34). Protection by other compounds such as ␣-ketoglutarate (22) and cocarboxylase (23) or by ischemic preconditioning (3) may be more efficient. The addition of adenosine to the cardioplegic solution or for pretreatment has not given conclusive effects so far (28,32,40).…”

mentioning

confidence: 99%

Myocardial interstitial glucose and lactate before, during, and after cardioplegic heart arrest

Kennergren

Mantovani

Strindberg³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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The interstitial fluid of the human myocardium was monitored in 13 patients undergoing aortic valve and/or bypass surgery before, during, and after hypothermic potassium cardioplegia. The regulation of glucose and lactate was studied after sampling with microdialysis. The following questions were addressed. 1) Is the rate of transcapillary diffusion the limiting step for myocardial uptake of glucose before or after cardioplegia? 2) Does cold potassium cardioplegia induce a critical deprivation of glucose and/or accumulation of lactate in the myocardium? Before cardioplegia, interstitial glucose was ∼50% of the plasma level ( P < 0.001). Interstitial glucose decreased significantly immediately after induction of cardioplegia and remained low (1.25 ± 0.25 mM) throughout cardioplegia. It was restored to precardioplegic levels 1 h after release of the aortic clamp. Interstitial glucose then decreased again at 25 and 35 h postoperatively to the levels observed during cardioplegia. Interstitial lactate decreased immediately after induction of cardioplegia but returned to basal level during the clamping period. At 25 and 35 h, interstitial lactate was significantly lower than before and during cardioplegia. Glucose transport over the capillary endothelium is considered rate limiting for its uptake in the working heart but not during cold potassium cardioplegia despite the glucose deprivation following perfusion of glucose-free cardioplegic solution. Lactate accumulated during cardioplegia but never reached exceedingly high interstitial levels. We conclude that microdialysis provides information that may be relevant for myocardial protection during open-heart surgery.

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Addition of α-Ketoglutarate to Blood Cardioplegia Improves Cardioprotection

Cited by 36 publications

References 17 publications

Protective role of pinacidil against adrenaline-induced myocardium injury in guinea pig liver mitochondria

Protective role of pinacidil against adrenaline-induced myocardium injury in guinea pig liver mitochondria

Alpha-ketoglutarate attenuates toxic effects of sodium nitroprusside and hydrogen peroxide in Drosophila melanogaster

Myocardial interstitial glucose and lactate before, during, and after cardioplegic heart arrest

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