Title
Effects of Chronic Lead Treatment on Some Cardiovascular Responses to Norepinephrine in the Rat
Author
Betty J. Williams, William H. Griffith III, Catherine M. Albrecht, James H. Pirch, Milton R
Publication
Toxicology and Applied Pharmacology, Volume 40, Issue 3, June 1977, pp. 407–413
Link
Abstract
Rats were treated with lead via the mother’s milk from birth to weaning. After a lead-free period of approximately 4 months, responses to norepinephrine were tested. Neither the pressor effect nor the enhancement of myocardial cAMP accumulation caused by norepinephrine was altered by prior lead treatment. However, norepinephrine caused significantly more cardiac arrhythmias in lead-treated animals than in controls. Even doses of norepinephrine which caused no significant ECG abnormalities in control animals were arrhythmogenic in lead-treated rats. It is concluded that lead treatment causes changes in cardiac conduction which are not readily reversed by termination of lead exposure.
Title
Lead Toxicity Treatment & Management
Author
Pranay Kathuria & Tarakad S Ramachandran
Publication
MedScape
Link
http://emedicine.medscape.com/article/1174752-treatment
Title
Emergent Management of Lead Toxicity
Author
Steven Marcus & Asim Tarabar
Publication
MedScape
Link
http://emedicine.medscape.com/article/815399-overview
Title
Lead Toxicity and Nutritional Deficiencies
Author
O A Levander
Publication
Environmental Health Perspective, 29: 115–125, Apr 1979
Link
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1637366/
Abstract
Under appropriate conditions, deficiencies of certain minerals and vitamins as well as high intakes of dietary fat increase the toxicity of a given dose of lead in experimental animals. The severity of lead poisoning can also be increased by the consumption of either deficient or excessive levels of protein. Mineral deficiencies appear to have some of the most profound effects on lead toxicity, since the consequences of plumbism can be exaggerated by feeding diets low in calcium, phosphorus, iron, zinc, and in some cases, copper. Evidence for an antagonism between lead and nutritional levels of selenium is inconclusive. Vitamin E deficiency and lead poisoning interact to produce an anemia in rats that is more severe than that caused by either treatment alone. Lead apparently exerts a pro-oxidant stress on the red cell, thereby causing its accelerated destruction. One of the biochemical mechanisms of lead poisoning may be the disruption of normal membrane architecture, thereby leading to peroxidative damage. Epidemiological surveys have suggested a negative correlation between the poor nutritional status of children with regard to calcium and the concentration of lead in blood. Other examples of potential interactions of mineral status and lead poisoning in humans include the hypothesized hazards of soft water to public health in areas with lead plumbing and the possible role of mineral deficiencies in the etiology of pica. Experimental studies have shown that in some situations combined nutritional deficiencies can have an additive effect in potentiating lead toxicity.