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ORIGINAL RESEARCH ARTICLE

Dietary Polyunsaturated Fatty Acids Alter Myocardial Protein Kinase C Expression and Affect Cardioprotection Induced by Chronic Hypoxia

Markéta Hlaváková^*,, Jan Necká^,, Jana Jeková^,, Patricie Balková, Barbora Staková^||, Olga Nováková^,, Frantiek Kolá^, and Frantiek Novák^*,1

^* Departments of Biochemistry and Animal Physiology, Faculty of Science, Charles University in Prague, Prague, Czech Republic; Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic; Centre for Cardiovascular Research, Prague, Czech Republic; and Fourth Department of Medicine, First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic

To whom requests for reprints should be addressed at ¹ Charles University, Faculty of Science, Department of Biochemistry, Hlavova 8, 128 43 Prague 2, Czech Republic. E-mail: franov{at}natur.cuni.cz

We examined the influence of dietary fatty acid (FA) classes on the expression of protein kinase C (PKC) and in relation to the cardioprotective effects of chronic intermittent hypoxia (CIH). Adult male Wistar rats were fed a nonfat diet enriched with 10% lard (saturated FA [SFA]), fish oil (n-3 polyunsaturated FA [n-3 PUFA]), or corn oil (n-6 PUFA) for 10 weeks. After 4 weeks on the diet, each group was divided into two subgroups that were either exposed to CIH in a barochamber (7000 m, 8 hrs/ day) or kept at normoxia for an additional 5–6 weeks. A FA phospholipid profile and Western blot analysis of PKC were performed in left ventricles. Infarct size was assessed in anesthetized animals subjected to 20-min coronary artery occlusion and 3-hr reperfusion. CIH decreased the n-6/n-3 PUFA ratio in all groups by 23% independently of the initial value set by various diets. The combination of n-3 diet and CIH had a stronger antiarrhythmic effect during reperfusion than the n-3 diet alone; this effect was less pronounced in rats fed the n-6 diet. The normoxic n-6 group exhibited smaller infarctions (by 22%) than the n-3 group. CIH decreased the infarct size in n-3 and SFA groups (by 20% and 23%, respectively) but not in the n-6 group. Unlike PKC, the abundance of PKC in the myocardial particulate fraction was increased by CIH except for the n-6 group. Myocardial infarct size was negatively correlated (r = – 0.79) with the abundance of PKC in the particulate fraction. We conclude that lipid diets modify the infarct size–limiting effect of CIH by a mechanism that involves the PKC-dependent pathway.

Key Words: chronic hypoxia • ischemia • infarction • protein kinase C • polyunsaturated fatty acids