Glucose, Insulin, Potassium Protection During the Course of Hypothermic Global Ischemia and Reperfusion

Heß, Michael; Okabe, Eiichiro; Poland, James L.; Warner, Mark; Stewart, James R.; Greenfield, L. J.

doi:10.1097/00005344-198301000-00005

Cited by 80 publications

(29 citation statements)

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“…It was possible to enhance the recovery of myocardial function with antioxidant drugs or enzymes able to scavenge free radicals during experimental heart ischaemia and reperfusion phase (Hess et al, 1983;Schlafer et al, 1982).…”

Section: Discussionmentioning

confidence: 99%

Effect of trimetazidine on membrane damage induced by oxygen free radicals in human red cells.

Maridonneau‐Parini¹,

Harpey²

1985

Brit J Clinical Pharma

144

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The effect of trimetazidine, 1‐(2, 3, 4 trimethoxybenzyl)piperazine di‐ hydrochloride, on membrane damage induced by oxygen free radicals in red cells was studied in seven healthy volunteers after oral administration. Red cells collected prior to and after a 7 day treatment period with trimetazidine were incubated in the presence of phenazine methosulphate (an intracellular oxygen free radical generator) and diethyldithiocarbamate (a Cu‐Zn superoxide dismutase inhibitor). The loss of intracellular K+ induced by oxygen free radicals and the membrane content of peroxidated lipids were significantly reduced in red cells collected after the period of treatment. These results indicate a potent antioxidant activity of trimetazidine which could explain its cardioprotective role during ischaemic and reperfusion phases in which oxygen free radicals are generated and probably implicated in the genesis of cardiac cell injury.

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Section: Discussionmentioning

confidence: 99%

Effect of trimetazidine on membrane damage induced by oxygen free radicals in human red cells.

Maridonneau‐Parini¹,

Harpey²

1985

Brit J Clinical Pharma

144

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“…ionic balance, membrane potential), particularly if the specific enzymes required for glucose breakdown exist in close proximity to the cell membrane (Runnman et al, 1990). In addition, exogenous glucose may further protect the in situ heart by acting as a free radical scavenger during reoxygenation (Hess et al, 1983). Although glucose uptake was not measured, it is possible that the in situ hearts used in this study had an enhanced rate of glucose uptake from the hypoxic perfusate compared to our previous studies (Arthur et al, 1992;Gamperl et al, 2001), and that this enhanced the post-hypoxic recovery of myocardial function.…”

Section: Potential Adaptations Mediating Hypoxia Tolerancementioning

confidence: 99%

All rainbow trout (Oncorhynchus mykiss) are not created equal:intra-specific variation in cardiac hypoxia tolerance

Faust

Gamperl

Rodnick

2004

Journal of Experimental Biology

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“…jury in the setting of ischemic heart disease gained widespread interest. Although most experimental studies demonstrated that glucose or GIK improved cardiac function and reduced injury during myocardial ischemia (5-12) or hypoxia (13)(14)(15)(16)(17)(18), clinical studies have yielded conflicting results (4,(19)(20)(21)(22)(23)(24)(25)(26). Some of the discrepancies may be related to the severity of ischemia, since in experimental studies the benefit of GIK during low-flow moderate ischemia was lost during severe ischemia (12), probably owing to more complete inhibition of anaerobic glycolysis and poorer delivery of substrate to the ischemic area.…”

Section: Introductionmentioning

confidence: 99%

“…For example, GIK has consistently been found to lower circulating levels of free fatty acids, which are known to be deleterious in the setting of myocardial ischemia, and this action has been proposed as an alternate explanation for the beneficial effects of GIK (7,9,10). Other potentially significant factors include preservation of cardiac glycogen stores (28-31), membrane-stabilizing effect of insulin (7,27), increased osmotic pressure (5), and free radical scavenging effects of glucose (18).…”

Section: Introductionmentioning

confidence: 99%

Enhanced utilization of exogenous glucose improves cardiac function in hypoxic rabbit ventricle without increasing total glycolytic flux.

Runnman¹,

Lamp²,

Weiss³

1990

J. Clin. Invest.

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The effects of elevated glucose on cardiac function during hypoxia were investigated in isolated arterially perfused rabbit interventricular septa. Rest tension, developed tension, intracellular potential, 42K' efflux, lactate production, exogenous glucose utilization, and tissue high-energy phosphate levels were measured during a 50-min period of hypoxia with 4, 5, or 50 mM glucose present (isosmotically balanced with sucrose) and during reoxygenation for 60 min with perfusate containing 5 mM glucose/45 mM sucrose. At physiologic (4 or 5 mM) and supraphysiologic glucose (50 mM), lactate production and high-energy phosphate levels during hypoxia were equally well maintained, yet cardiac dysfunction was markedly attenuated by 50 mM glucose. Despite identical rates of total glycolytic flux, exogenous glucose utilization was enhanced by 50 mM glucose so that tissue glycogen levels remained normal during hypoxia, whereas glycogen became depleted with 4 or 5 mM glucose present during hypoxia. Most of the beneficial effects of 50 mM glucose occurred during the first 25 min of hypoxia. Prior glycogen depletion had no deleterious effects during hypoxia with 50 mM glucose present, but exacerbated cardiac dysfunction during hypoxia with 5 mM glucose present. These findings indicate that enhanced utilization of exogenous glucose improved cardiac function during hypoxia without increasing total glycolytic flux or tissue high-energy phosphate levels, suggesting a novel cardioprotective mechanism. (J.

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Glucose, Insulin, Potassium Protection During the Course of Hypothermic Global Ischemia and Reperfusion

Cited by 80 publications

References 1 publication

Effect of trimetazidine on membrane damage induced by oxygen free radicals in human red cells.

Effect of trimetazidine on membrane damage induced by oxygen free radicals in human red cells.

All rainbow trout (Oncorhynchus mykiss) are not created equal:intra-specific variation in cardiac hypoxia tolerance

Enhanced utilization of exogenous glucose improves cardiac function in hypoxic rabbit ventricle without increasing total glycolytic flux.

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