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  • Title: [Protective effect of endogenous catecholamine depletion against hypoxic and reoxygenation damage in isolated rat heart: an ultrastructural study (author's transl)].
    Author: Feuvray D, James F, de Leiris J.
    Journal: J Physiol (Paris); 1980; 76(7):717-22. PubMed ID: 7218160.
    Abstract:
    Using isolated, Langendorff-perfused rat hearts, we studied in the left ventricular wall myocardial ultrastructural modifications appearing under conditions of severe hypoxia and subsequent reoxygenation. Hypoxia was produced by gassing perfusate with nitrogen (aortic oxygen partial pressure less than 8 mmHg). The purpose of the present work was to evaluate whether or not endogenous catecholamines might be involved in the development of hypoxia-induced tissue damage isolated heart. Therefore, severe hypoxia and subsequent reoxygenation was studied using hearts isolated from (a) normal untreated rats, and (b) from rats in which endogenous catecholamine levels have been reduced to about 15% of control values by reserpine (2 I.P. injections: 1.5 mg/kg 48 hours, and 5 mg/kg 24 hours prior to the excision of the heart). Hearts were fixed by glutaraldehyde perfusion either after 10 min of control equilibration perfusion (with oxygen and glucose), or after 100 min hypoxia (nitrogen, glucose-free, high potassium), or after hypoxia plus reoxygenation (oxygen, substrate-free, high potassium). After fixation, dehydration, embedding in araldite, 6-8 blocks per heart were sectioned; the sections were doubly stained and examined under the electron microscope. 1. Control hearts perfused for a 10 min equilibration period exhibited well preserved and normal ultrastructure (Fig. 1). This observation indicated that our experimental conditions of perfusion were able to maintain the ultrastructural integrity of the myocardium satisfactorily, and that the fixation procedure used was correct. After severe hypoxia without substrate, untreated hearts exhibited ultrastructural alterations, the degree of which was consistently and severely increased by reoxygenation (Figs. 2 and 3). 2. In reserpine pretreated hearts, in which we observed a marked increase in the number of glycogen granules (Fig. 4), hypoxia did not induce morphological alterations. Even after 100 min hypoxia, some glycogen granules were still visible (Fig. 5). Furthermore, myocardial ultrastructure was not altered by reoxygenation (Fig. 6). It is proposed that in reserpine pretreated hearts, anaerobic metabolism of glycogen may be sufficient to sustain enough glycolytic ATP production during 100 min of oxygen deprivation. Such a preservation of myocardial high-energy phosphates could help myocardial cells to maintain their structural integrity. These results are discussed in connection with those of a previous biochemical study of reserpine's protective action in hypoxic isolated rat hearts.
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