Influence of long-term supplementation with alpha-linolenic acid on myocardial lipid peroxidation and antioxidative capacity in spontaneously hypertensive rats.

The ischaemic vulnerability of the heart of spontaneously hypertensive rats (SHR) is enhanced after feeding an alpha-linolenic acid (LNA) enriched diet. Because oxygen radical-induced reactions (e.g.

Prenatal hypoxia alters the postnatal development of beta-adrenoceptors in the rat myocardium.

The effect of prenatal hypoxia on the development of the beta-adrenoceptor during the ontogenesis of rats was investigated. It was shown that the offspring from hypoxic dams, in comparison with normoxic control animals, exhibited alterations of the density (Bmax) of the myocardial beta-receptors and of the catecholamine levels in heart tissue during development. The results suggest that the beta-adrenoceptor changes might be involved in the phenomenon of enhanced sensitivity of prenatal hypoxic animals to catecholamines in adult age.

The catecholamine sensitivity of adult rats is enhanced after prenatal hypoxia.

In this study, the effect of prenatal hypoxia on the catecholamine sensitivity of the offspring of pregnant rats was investigated. The offspring from hypoxic animals showed after treatment with isoproterenol in adult age a distinctly more pronounced decrease of protein content and enzyme activities in heart tissue as well as a significantly higher elevation of enzyme activities in blood plasma as compared with the offspring from normoxic rats. These results suggest a long-lasting enhancement of catecholamine sensitivity after prenatal oxygen deficiency.

In vitro effects of reactive O2 species on the beta-receptor-adenylyl cyclase system.

The irreversible loss of activity of the sarcolemma-localized beta-receptor-adenylyl cyclase system (beta-RAS) in myocardial ischemia is a well documented phenomenon. Alterations in the sarcolemma (SL) induced by reactive O2 species could be responsible for this loss. Therefore the influence of oxidation of SH-groups and lipid peroxidation induced by Fe2+/Vit.

Arachidonic acid metabolism in cultured adult myocardial cells under short-time hypoxic conditions.

The present study utilized a cultured adult myocardial cell model to examine the arachidonic acid metabolism under different cell-damaging and normoxic conditions. Cell injury was caused by short-time hypoxia, calcium ionophore A 23187-triggered cell-damage under hypoxia and cell disruption by freezing and thawing. The current study demonstrates that under the cell-damaging conditions cultured adult heart myocytes resemble myocardial cells under normoxic conditions in metabolizing arachidonic acid into triacylglycerols and phospholipids as the major route (a), in formation of ETYA-inhibitable indomethacin-resistant lipid metabolites in minor amounts (b) and in being independent of calcium overload in the metabolic pathways of arachidonic acid metabolism (c).