Chronic Effects of Mercury on Organisms:

Cardiotoxic effects of mercury


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CARDIOTOXIC EFFECTS OF MERCURY Summary only The obtained data indicates that, in experimental animals, coronary insufficiency develops at lower pituitin doses, and changes are more pronounced than in controls. We obtained some EKG's and data from separate experiments illustrating the differences in coronary spasm development in test and control animals. In conclusion, let us stress that, in this series of experiments, there was notable variability in individual sensitivity of rabbits to pituitrin. In some cases, the same animal responded differently to separate pituitrin injections while in others response to pituitrin was less marked. However, despite individual variations, in an overwhelming majority of cases in animals subjected to prolonged mercury exposure, EKG shifts were more sharply developed than in control rabbits. One can speak of the mechanism of growing myocardial hypoxia leading to acute coronary spasm under the influence of pituitrin. On the other hand, coronary vascular spasm might not be developed enough, appearing only under the influence of mercury, but even minor spasms could disrupt myocardial trophics, both factors reflecting in the EKG, and both obviously playing a determining role. Low intensity toxic effects can make simultaneous background metabolic changes and produce significant circulatory changes. During prolonged exposure to mercury a number of changes in different parts of the self-regulatory functions of the circulatory system occur. Reactivity of cardiac effecters, tonic affects in sympathetic and parasympathetic innervation centers appear. These shifts in interaction of the center and periphery include respective feedback information, thereby establishing a new level of cardiovascular self-regulation. Currently, much attention is paid to facilitating reactions, compensatory reserve mechanisms of one or another system. Our data shows that prolonged exposure even to low mercury intensities (about 0.01 mg/m3) limit cardiovascular reactive capability. We feel that this conclusion should have principal significance in general analysis of pathological changes appearing in the organism under the influence of low concentrations of toxic substances.