The aim of this study was to investigate whether chronic (1, 3, 6, 12, or 16 months) low lead (5 or 25 ppm), administered as lead acetate in the drinking water, commencing either after weaning or from conception, altered the susceptibility of the heart to arrhythmias induced by coronary artery ligation in pentobarbitone anesthetized male Sprague-Dawley rats. The cardiac effects of chronic (3 or 12 months) administration of lead (25 ppm) were also examined in spontaneously hypertensive rats. Treatment from weaning of normotensive rats with 5 or 25 ppm lead for periods of 1, 3, or 6 months had no statistically significant effect on the severity of ischemia-induced arrhythmias. Each of the groups treated from conception with 5 or 25 ppm lead for periods of 1, 12, or 16 months exhibited a higher incidence of ventricular tachycardia than the appropriate control group, but the difference was statistically significant only in the case of animals treated with 25 ppm lead for 12 months. The incidence of ventricular fibrillation was significantly higher in rats treated from conception for 16 months with 5, but not with 25 ppm lead. Spontaneously hypertensive rats treated with 25 ppm lead for 3 but not for 12 months had significantly more ectopic beats than control Sprague-Dawley rats. Lead treatment for the longer exposure periods only caused significant accumulation of lead in the blood whereas all lead treatments resulted in a marked accumulation in the bone. We conclude that chronic exposure to low concentrations of lead does not consistently alter susceptibility of the heart to ischemia-induced arrhythmias in anesthetized rats.
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