期刊
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
卷 282, 期 1, 页码 E197-E206出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.2002.282.1.E197
关键词
fatty acids; glucose; lactate; oxidation; heart
资金
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL043023, R01HL058653, R01HL064848, R01HL062573] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL-64848, R01 HL-58653, R01 HL-62573, P01 HL-43023] Funding Source: Medline
To test whether the acute reduction of nitric oxide (NO) synthesis causes changes in cardiac substrate metabolism and in the activity of key enzymes of fatty acid and glucose oxidation, we blocked NOS by giving N-omega-nitro-L-arginine methyl ester (L-NAME; 35 mg/kg iv two times) to nine chronically instrumented dogs. [H-3] oleate, [C-14] glucose, and [C-13] lactate were infused to measure the rate of cardiac substrate uptake and oxidation. Glyceraldehyde-3-phosphate dehydrogenase, acetyl-CoA carboxylase, and malonyl-CoA decarboxylase activities were measured in myocardial biopsies. In eight control dogs, ANG II was infused (20-40 ng.kg(-1).min(-1)) to mimic the hemodynamic effects of L-NAME. After L-NAME, significant changes occurred for fatty acid oxidation (from 9.8 +/- 0.8 to 7.1 +/- 1.2 mu mol/min), glucose uptake (from 12.9 +/- 5.5 to 45.0 +/- 14.2 mu mol/min), and oxidation (from 4.4 +/- 1.2 to 19.9 +/- 2.3 mu mol/min). ANG caused only a significantly lower increase in glucose oxidation. Lactate uptake increased by more than twofold in both groups. The enzyme activities did not differ significantly between the two groups. In conclusion, the acute inhibition of NO synthesis causes marked metabolic alterations that do not involve key rate-controlling enzymes of fatty acid oxidation nor glyceraldehyde-3-phosphate dehydrogenase.
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