The goal of this review is to present a comprehensive survey of the many intriguing facets of creatine (Cr) and creatinine metabolism, encompassing the pathways and regulation of Cr biosynthesis an...

http://www.afboard.com/library/creatinemetabolism.pdf

Creatine and Creatinine Metabolism

Utilization of carbohydrate and fatty acids is strongly influenced by rates of con­ sumption and production of high energy compounds in cardiac muscle. In well­ oxygenated hearts, fatty acid has been identified as the preferred substrate by both in vivo and in vitro studies (for review see 146). Availability of fatty acid suppresses glucose utilization by inhibition of several steps in the glycolytic pathway. Since a variety of longand short-chained fatty substrates are inhibitory and since the effect is abolished in hearts perfused under anaerobic conditions, oxidation of the fatty acid appears to be required for this effect. When energy utilization of well­ oxygenated hearts is increased, consumption of fatty acids and/or glucose is ac­ celerated. Under these conditions, fatty acids remain the preferred oxidative substrate. Availability of oxygen to the heart can be restricted either by lowering or reducing to zero the oxygen tension of the perfusate, thereby inducing hypoxia or anoxia, or by restricting the flow of perfusate containing high oxygen tensions to induce ischemia. In hypoxic or anoxic hearts, fatty acid oxidation is suppressed and glycol­ ysis is stimulated. The acceleration of flux through glycolysis may be as much as 10to 20-fold. On the other hand, ischemia results in only a transient increase in glycolytic flux that is followed within 3-4 min by inhibition. Fatty acid oxidation is suppressed in ischemic hearts leading to accumulation of long-chained CoA derivatives and increase in triglyceride levels.

Relationship Between Carbohydrate and Lipid Metabolism and the Energy Balance of Heart Muscle

The relationship between progressive depletion of high energy phosphate and the onset of lethal cell injury in ischemic myocardium following coronary occlusion has been evaluated. Myocardial ischemia was induced by proximal occlusion of the circumflex coronary artery for 15, 30, 40, or 60 minutes. Cell injury in the severely ischemic posterior papillary muscle (PP) was evaluated by electron microscopy and by measuring the capacity of slices of the injured PP to maintain electrolytes, resynthesize high energy phosphate, and exclude inulin during in vitro incubation. ATP content in the ischemic myocardium decreased to 35%, 9%, 7%, and 5% of control values after 15, 30, 40, and 60 minutes of ischemia, respectively, and was associated with a corresponding depletion of total adenine nucleotides. The loss of 65% of the ATP after 15 minutes of ischemia (reversible injury) was associated with only minimal ultrastructural changes and no significant defects of electrolytes in incubated slices. However, the depletion of over 90% of the ATP after 40 minutes of ischemia (irreversible injury) was associated with significant fine structural changes and markedly altered cell volume regulation. The results suggest a close relationship between the marked depletion of high energy phsophates and the development of lethal injury in acutely ischemic myocardium.

Relation between high energy phosphate and lethal injury in myocardial ischemia in the dog.

http://msg2018.weebly.com/uploads/1/6/1/0/16101502/jaswal_2011_targeting_fatty_acid_and_carbohydrate_oxidation___a_novel_therapeutic_intervention_in_the_ischemic_and_failing_heart__.pdf

Targeting fatty acid and carbohydrate oxidation--a novel therapeutic intervention in the ischemic and failing heart.

The subendocardial to subepicardial gradient in the severity of ischemia following acute coronary occlusion is described. The effects of mild, moderate, and severe ischemia on cell structure and function are compared in summary form, and special attention is given to the effects of severe ischemia on myocardial cells. The characteristics of reversible and irreversible ischemic injury are defined in biologic terms. The failure of cell volume regulation in cells which have entered an irreversible state of ischemic injury is demonstrated by the use of free-hand slices in vitro. Irreversibility is associated with structural defects in the plasma membrane and is reflected in an increased slice inulin-diffusible space, increased slice H2O and Na+ content, and failure of the tissue to maintain the high K+ and Mg2+ levels characteristic of normal left ventricular myocardium. Defective cell membrane function is an early feature of irreversible ischemic injury and may be a primary event in the genesis of the irreversible state.

Ischemic tissue injury.

The relationship between coronary flow and adenosine triphosphate ATP production was determined in isolated rat hearts and in situ pigs hearts. The major source of ATP in ischemic hearts was oxidative phosphorylation. Oxidation of glucose accounted for most of the residual oxygen consumption in ischemic hearts when the concentration of fatty acids was low, but at 1.2 mM palmitate fatty acids were oxidized in preference to carbohydrate, as in aerobic hearts. The rates of ATP production from both glycolysis and oxidative metabolism were decreased in proportion to the reduction in coronary flow in oxygen-deficient hearts. Glycolysis was reduced to below aerobic rates when coronary flow was about 0.5 ml/min/g tissue in both rat hearts perfused with bicarbonate buffer and blood-perfused pig hearts. Tissue level of high energy phosphates reflected the rates of ATP production and declined in proportion to the reduction in coronary flow. In addition, tissue lactate and H+ accumulated in proportion to the restriction in flow.

Relationship between coronary flow and adenosine triphosphate production from glycolysis and oxidative metabolism.

Rates of glycolysis were determined in the isolated perfused rat heart under aerobic, anoxic, and ischemic conditions. The rate was accelerated in anoxic and was inhibited in ischemic tissue. Glycolytic inhibition developed at the level of glyceraldehyde-3-P dehydrogenase and was associated with accumulation of high levels of tissue lactate and H+.

Inhibition of glycolysis in hearts during ischemic perfusion.

NEELY, J. R., M. J. ROVETTO, J. T. WHITMER, AND H. IL MORGAN. Effects of ischemia on function and metabolism of the isolated wcrking rut heart. Am. J. Physiol. 225(3): 651-658. 1973.-Two techniques have been developed for inducing whole-heart ischemia in the isulated working rat heart, These procedures allowed total coronary Aow to be reduced in hearts that were performing external mechanical work. Reducing the rate of coronary flow resulted in myocardial ischemia as indicated by reduced oxygen delivery and consumption, increased production, and tissue accumulation of lactate, and ventricular failure. A 50y0 reduction in coronary flow resulted in ventricular failure within 8 min. Metabolism of the ischemic hearts was characterized by depletion of tissue highenergy phosphates and accumulation of ADP and AMP. Within 2 min, creatine phosphate and ATP had decreased by 70 and 2597,, respectively, and the level of ADP had increased by 100 %. After 20 min of ischemia, tissue levels of ATP had decreased by 70%, ADP had returned to control levels, and AMP had increased about fivefold. Irreversible ventricular failure occurred in 50 and 100% of the hearts after exposure to about 20 and 30 min of ischemia, respectively,

Effects of ischemia on function and metabolism of the isolated working rat heart.

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Relationship between coronary flow and adenosine triphosphate production from glycolysis and oxidative metabolism.

Inhibition of glycolysis in hearts during ischemic perfusion.

Effects of ischemia on function and metabolism of the isolated working rat heart.