Abstract
1. The effect of the calcium channel blocker nisoldipine on the myocardial content of lipid peroxidation products (malondialdehyde (MDA), conjugated double bonds (CDB), fluorescent end-products (RF) and mitochondrial adenine nucleotides) was investigated in conscious pigs (n = 14) subjected to 24 h of immobilization stress. Histoenzymatic and electron microscopic studies of the myocardium were also performed. Nisoldipine was given orally in a twice daily dose of 20 mg for 2 days before and on the day of the experiment. Results were compared with those obtained in immobilized untreated pigs (n = 10) and in non-stressed treated controls (n = 8). 2. Pretreatment with nisoldipine significantly attenuated stress-induced increase in myocardial contents of CDB and RF and prevented decline of mitochondrial adenine nucleotides. Stress-induced myocardial histoenzymatic changes (decrease of succinic dehydrogenase, ATPase, acid phosphatase activity) and ultrastructural alterations (mitochondrial damage, lysis of myofibrils, dilatation of sarcoplasmic reticulum and endothelial swelling) were also diminished. 3. It is concluded that treatment with a Ca2(+)-antagonist is beneficial to the heart exposed to environmental stress.
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