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The effects of exposure to extremely low frequency electric fields (ELF EFs) on plasma lipid peroxide levels and antioxidant activity (AOA) in Sprague-Dawley rats were studied. The test was based on comparisons among rats treated with a combination of the oxidizing agent, 2,2'-azobis(2-aminopropane) dihydrochloride (AAPH) and 50 Hz EF of 17.5 kV/m intensity for 15 min per day for 7 days, AAPH alone, EF alone or no treatment. EF significantly decreased the plasma peroxide level in rats treated with AAPH, similar to treatment by ascorbic acid or the superoxide dismutase. Ascorbic acid increased AOA; however, EF and superoxide dismutase did not change AOA compared with sham exposure in stressed rats. No influence on the lipid peroxide level and AOA in unstressed rats was observed with EF exposure alone. Although the administration of AAPH decreased AOA, this decrease did not change when EF was added. These data indicate that the ELF EF used in this study influenced the lipid peroxide level in an oxidatively stressed rat.

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In rabbits and rats, both stimulation of alpha-adrenoceptors and ischemic preconditioning (PC) reduce infarct size. Activation of alpha1b-adrenoceptors play an important role in the PC effect on ventricular function in rats. However, the alpha1-adrenoceptors have not been reported to be related to the PC effect in rabbits, because the infarct size-reducing effect of PC is not blocked by the nonselective alpha-adrenoceptor antagonist, phenoxybenzamine (POB) or by the alpha1-adrenoceptor antagonist, BE2254. However, we speculated that alpha1b-adrenoceptors but not alpha1a-adrenoceptors may be related to the infarct size-reducing effect of PC in rabbit hearts. Thus we examined in rabbits whether the alpha1b-adrenoceptor blocker chloroethylclonidine (CEC), the alpha1a-adrenoceptor blocker 5-methylurapidil (5-MU), the selective alpha1-adrenoceptor antagonist bunazosin (BN), and the nonselective apha-adrenoceptor antagonist phenoxybenzamine (POB) can block the PC effect on infarct size. Eighty-eight anesthetized open-chest Japanese white male rabbits were subjected to 30-min coronary occlusion and 48-h reperfusion. In five PC groups, the rabbits were subjected to a single 5-min occlusion and 5-min reperfusion before 30-min sustained ischemia. In the PC groups, those with CEC (3 mg/kg, n = 10), 5-MU (3 mg/kg, n = 10), BN (0.3 mg/kg, n = 10), POB (4 mg/kg, n = 10), or placebo saline (n = 10) were pretreated before PC. In the non-PC groups, those with CEC (3 mg/kg, n = 7), 5-MU (3 mg/kg, n = 7), BN (0.3 mg/kg, n = 7), POB (4 mg/kg, n = 7), or placebo saline (n = 10) were pretreated before 30-min sustained ischemia. After a 48-h reperfusion, the infarct size was measured histologically and expressed as a percentage of the area at risk. PC caused a marked reduction of infarct size as compared with the non-PC control (10 +/- 3% vs. 42 +/- 2%; p < 0.05). The PC effect was completely blocked by CEC (36 +/- 2%) and by BN (42 +/- 4%) but not by 5-MU (14 +/- 1%) or POB (13 +/- 2%). None of the drugs by itself affected the infarct size. Stimulation of alpha1b-adrenoceptors but not of alpha1a-adrenoceptors during PC plays an important role in the PC effect on infarct size. This may explain the previous confusion concerning the PC blocking effect of various alpha1-blockers.