Abstract：
:In response to a prolonged pressure- or volume-overload, alterations occur in myocardial fatty acid, glucose, and glycogen metabolism. Oxidation of long chain fatty acids has been found to be reduced in hypertrophied hearts compared to non-hypertrophied hearts. However, this observation depends upon the degree of cardiac hypertrophy, the severity of carnitine deficiency, the concentration of fatty acid in blood or perfusate, and the myocardial workload. Glycolysis of exogenous glucose is accelerated in hypertrophied hearts. Despite the acceleration of glycolysis, glucose oxidation is not correspondingly increased leading to lower coupling between glycolysis and glucose oxidation and greater H(+) production than in non-hypertrophied hearts. Although glycogen metabolism does not differ in the absence of ischemia, synthesis and degradation of glycogen are accelerated in severely ischemic hypertrophied hearts. These alterations in carbohydrate metabolism may contribute to the increased susceptibility of hypertrophied hearts to injury during ischemia and reperfusion by causing disturbances in ion homeostasis that reduce contractile function and efficiency to a greater extent than normal. As in non-hypertrophied hearts, pharmacologic enhancement of coupling between glycolysis and glucose oxidation (e.g., by directly stimulating glucose oxidation) improves recovery of function of hypertrophied hearts after ischemia. This observation provides strong support for the concept that modulation of energy metabolism in the hypertrophied heart is a useful approach to improve function of the hypertrophied heart during ischemia and reperfusion. Future investigations are necessary to determine if alternative approaches, such as glucose-insulin-potassium infusion and inhibitors of fatty acid oxidation (e.g., ranolazine, trimetazidine), also produce beneficial effects in ischemic and reperfused hypertrophied hearts.
journal_name
Heart Fail Revjournal_title
Heart failure reviewsauthors
Sambandam N,Lopaschuk GD,Brownsey RW,Allard MFdoi
10.1023/a:1015380609464subject
Has Abstractpub_date
2002-04-01 00:00:00pages
161-73issue
2eissn
1382-4147issn
1573-7322journal_volume
7pub_type
杂志文章,评审abstract：:Acute heat failure syndromes are a heterogenous group of conditions. Chronic heart failure exacerbations represent the vast majority of cases. Pathophysiologic mechanisms, such as hypotension with peripheral tissue hypoperfusion, renal function impairment and myocardial ischemia and injury, adversely affect patients' ...
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journal_title：Heart failure reviews
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journal_title：Heart failure reviews
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journal_title：Heart failure reviews
pub_type： 杂志文章,评审
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journal_title：Heart failure reviews
pub_type： 杂志文章,评审
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journal_title：Heart failure reviews
pub_type： 杂志文章,评审
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journal_title：Heart failure reviews
pub_type： 杂志文章,评审
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journal_title：Heart failure reviews
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pub_type： 杂志文章,评审
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journal_title：Heart failure reviews
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