Stress and Dietary Fat Influence Cell Membranes and Death Due to Ventricular Fibrillation and Heart Failure
Adaptation to chronic stress or repeated adrenergic stimulation, to dietary fat and ageing was accompanied by significant changes in fatty acyl chain profile of cell membranes in the heart. Changes in fatty acyl composition of membrane phospholipids preceded down-regulation of adrenoceptors or occurred simultaneously. Successful adaptation to stress was accompanied by a balance between 20:4n-6 and 22:6n-3 in membrane phospholipids. Increased intake of 22:6n-3 in form of cod liver oil resulted in diminished levels of 20:4n-6 in heart muscle and gastric mucosa. Reduced levels of 20:4n-6 in membrane phospholipids of both gastric mucosa and cardiac muscle increased the vulnerability of the tissue to stress induced necrosis. Sudden death in man was, on the other hand, frequently accompanied by low levels of 22:6n-3 in heart muscle and high ratio of 20:4n-6/22:6n-3. Sudden death in rats, due to ventricular fibrillation, could be significantly reduced by dietary cod liver oil and increased availability of 22:6n-3. The one factor that seems to be of major importance in stress tolerance is the cellular availability of both arachidonic acid and docosahexaenoic acid and the balance between these two competing fatty acids. The availability of these fatty acids for diverse regulatory functions can be influenced by well known risk factors of coronary artey disease such as chronic stress, dietary fat and ageing.
Key wordsStress omega-3 and omega-6 fatty acids membrane phospholipids adrenoceptors heart disease
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