Key result
Fenitrothion increases Ca45 influx, causing QT prolongation and electrolyte imbalances in guinea pigs.
Why the study?
The effects of fenitrothion on muscarinic acetylcholine receptor content and calcium influx in guinea pig heart tissue were not well characterized.
Chronic exposure to the acetylcholinesterase inhibitor fenitrothion in a guinea pig model induces significant cardiac electrolyte shifts, altered calcium influx, and arrhythmogenic electrocardiographic changes.
Animal data link fenitrothion to electrolyte shifts and QT prolongation; hypothesis-generating for human arrhythmic risk, should not change practice.
Fenitrothion is a powerful acetylcholinesterase inhibitor in turn causing increase in acetylcholine levels. The relationship between Ca45 influx and 3HQNB binding in the heart tissue of guinea pigs have been studied after intraperitoneal doses of Fenitrothion for a period of 1 month. A good correlation was observed between the increase of serum calcium levels and increase Ca45 influx. There was hypokalaemia and hypernatraemia in the serum, whereas marked decrease in PO2 and in PCO2 levels. Electrocardiogram revealed decrease in PR, and RR intervals and QT prolongation. Extrasystoles are also present.
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Anand et al. (1990) studied this question. Fenitrothion was evaluated on Ca45 influx and 3HQNB binding in the heart tissue. Intraperitoneal Fenitrothion for 1 month in guinea pigs increased Ca45 influx, correlated with increased serum calcium, and caused hypokalaemia, hypernatraemia, and QT prolongation.
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