Introduction: Acetaminophen is the most widely used over-the-counter drug in the
world as an analgesic and antipyretic, and although it is considered safe when used in
therapeutic doses, it is responsible for the most common causes of drug intoxication,
which can occur due to intentional or unintentional overdose, and may result in liver
failure and electrophysiological changes. Objective: To identify the occurrence of
electrocorticographic, electrocardiographic, and hepatic alterations in wistar rats
induced to paracetamol intoxication. Methods: Experimental design study using male
Wistar rats weighing 200-230g. The animals were divided into the following groups: A
- control with 0.9% saline solution via gavage (n=9); B - acetaminophen group,
receiving 1g/kg of acetaminophen orally (n=9). Electrocortigraphic,
electrocardiographic records and liver enzymes (AST and ALT) were performed in the
periods of 24, 48, 72 and 96 hours after drug administration. Results: A progressive
reduction in electrocorticography power was observed according to the progression of
observation time after acetaminophen administration. In the group treated with the
drug, the mean power was about 50% lower in the amplitude of brain oscillations
compared to the control. In all wave types (alpha, beta, delta, gamma, and theta) there
was a significant difference at 96 hours after application. As for the
electrocardiographic record, in the acetaminophen group, a decrease in cardiac activity
and alterations in the RR, PQ, and QT follow-up were observed after 72 and 96 hours,
in addition to an increase in the QRS duration as of 48 hours after the administration
of the acute toxic dose, maintaining sinus rhythm. In the study it was also identified
changes in the shape of the T wave, which showed greater irregularities and opening.
Finally, it was observed an increase in the activities of AST and ALT transaminases,
configuring liver damage with the dosage used in the study. Conclusion: In the central
nervous system, there was a progressive reduction in the amplitude of all brain waves
on electrocorticography (delta, theta, beta and gamma), with the exception of the alpha
wave, which showed increased activity. The reduction of most brain waves
corroborates the idea that the drug acts as an inhibitor of the central nervous system,
corresponding to the central analgesic effects promoted by it. Regarding
hepatotoxicity, the alterations described corroborate the liver damage, already widely
known, resulting from the toxicity of acetaminophen, demonstrated by the increase in
the levels of AST and ALT transaminases. Regarding the electrocardiographic
changes, there was a reduction in cardiac activity and changes in the
electrocardiographic segments, maintaining sinus rhythm. All the variables analyzed
showed their most significant changes after 72h of the administration of the toxic dose
of acetaminophen.
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