ISSN:
1435-1803
Keywords:
Hypoxia
;
glycerol
;
lipolysis
;
heart
;
catecholamines
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary Factors controlling hypoxia-induced myocardial glycerol release were studied in isolated, perfused rat hearts. A constant coronary flow rate 10 ml g−1 min−1 was maintained. The perfusion buffer was gassed with O2−N2 mixtures containing 5% CO2. The O2∶N2 ratios were normoxia 95∶0, hypoxia 30∶65, and severe hypoxia 10∶85 (v/v). Glycerol and lactate release were stimulated during a 30-min period of either hypoxia or severe hypoxia but remained constant during normoxia. Tissue glycerol-3-phosphate levels were increased after 30 min hypoxia compard with after a similar period of normoxic perfusion (p〈0.01) and further increased after severe hypoxia (p〈0.01 vs hypoxia). β-Adrenoceptors remained sensitive to isoprenaline during hypoxia, demonstrated by an increase in glycerol release over a 30-min period of isoprenaline infusion from 897±317 to 1771±307 nmol g−1 wet weight (p〈0.05). The isoprenaline-induced increase in glycerol release during hypoxia was inhibited by both atenolol and timolol (1×10−5M). In contrast, β-adrenoceptor blockade using these drugs failed to reduce glycerol release induced by either hypoxia or severe hypoxia. Both drugs attenuated the rise in glycerol-3-phosphate during hypoxia. Chronic denervation by pretreatment with 6-hydroxydopamine reduced hypoxia-stimulated glycerol release by only 30%. Thus, a major part of hypoxia-induced glycerol release is mediated by non-adrenergic mechanisms. The results of this study bring into question the validity of the use of glycerol production during hypoxia as a reliable measure of myocardial lipolysis.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00788675
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