We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Prilocaine induced epileptiform activity and cardiac toxicity is alleviated by thymoquinone treatment.
- Authors
Yıldırım, Sendegül; Tanrıöver, Gamze; Akgül, Barış; Aycan, İlker Öngüç; Hidişoğlu, Enis; Afşar, Ebru; Aslan, Mutay
- Abstract
Objective: The aim of this study was to investigate whether thymoquinone (TQ) could alleviate prilocaine-induced (PRL) central nervous system, cardiovascular toxicity in anaesthetized rats. Methods: With the approval of the Local Ethics Committee of the Animal Experiments of Akdeniz University; Rats were randomized to following groups: Control, PRL, TQ, PRL+TQ treated. Rats were anesthetized intraperitoneally. Fronto-occipital EEG and ECG electrodes were placed and the trachea was intubated. Mechanical ventilation was initiated with a tidal volume of ' 0 mg/kg and a rate of 50-55 breaths/min. Right femoral artery was cannulated for continuous blood pressure measurements and blood-gas sampling while the left femoral artery was cannulated for PRL infusion (8 mg/kg/min).TQ was given by gavage (15 mg/kg per day) for 3 days prior to drug administration. Arterial blood sample for blood gas analysis was drawn before drug infusion, during drug infusion and after cardiac arrest. Markers of myocardial injury, oxygen/nitrogen species generation, total antioxidant capacity were assayed by standard kits. AQP4, NFKBp65, p50 subunit in brain tissue were evaluated by immunohistochemically. Results: Blood pH,partial oxygen pressure was significantly decreased after PRL infusion. The decrease in blood pH was alleviated in the PRL+TQ group.PRL produced seizure activity on EEG at significantly lower doses compared to PRL+TQ rats. Cardiac arrhythmia, asystole on ECG occured at significantly lower doses in the PRL. PRL caused as significant increase in serum myoglobin, CK-MB levels. PRL+TQ treatment attenuated levels of myocardial injury.PRL caused increased ROS/RNS formation and decreased TAC in the heart, brain tissues.TQ increased heart, brain TAC and decreased ROS/RNS formation in PRL groups. AQP4, p50, p65 expressions were increased in cerebellar, cerebral cortex, choroid plexus in PRL treated rats. PRL+TQ decreased the expression of AQP4, p50, p65 in brain tissue (p<0.05). One-way Anova test was used for statistical significance between groups. Conclusion: The data shows that TQ is a protective agent against prilocaine-induced CNS and cardiovascular toxicity.TQ could ameliorate CNS and cardiac toxicity induced by high dose PRL treatment.
- Subjects
THERAPEUTICS; OXIDANT status; BIOPOTENTIALS (Electrophysiology); CENTRAL nervous system; ARRHYTHMIA; CEREBRAL cortex
- Publication
Anatomy: International Journal of Experimental & Clinical Anatomy, 2019, Vol 13, Issue S1, pS31
- ISSN
1307-8798
- Publication type
Article