electrocardiography

Carazolol is a non-specific β-adrenargic reseptor blocking agent. It ıs structurally analogous to catecholamins, in that, when administered, it forms reversible bonds with β-adrenergic, however, induce adrenergic effects, and it inhibits the actions of the catecholamins in times of stres by saturing their sites of operation. The purpose of the research was to investigate the effects of carazolol on some serum enzymes, trace elements and cardiovascular status in sheep. Seven sheeps (age 6 months, 35 ± 10 kg) were used in this study. Carazolol administered by the intramuscular route at the dose of 0.01 mg/kg. Serum levels of urea, creatinin, ALT, AST, G-GT, LDH, T. protein, Ca, P, Mg, Cu, Fe, Zn, Se were investigated. Although all serum enzymes did not show any difference, serum Fe and Zn levels were decreased. Important results were obtained in electrocardiography (abnormal T wave and ST segment depression). These results suggest that carazolol may increase incidence rate of myocardiyal ischemia risk in sheeps and it investigated by new researches.

Background: Studies explored the therapeutic role of agents inhibiting RAS in epilepsy. Fewer studies addressed the electrophysiological changes associated with angiotensin converting enzyme inhibitors (ACEIs) in terms of sustained seizures (status epilepticus). Sodium valproate (SVPA), a broad-spectrum anticonvulsant, has been associated with adverse cardiac events upon long-term use, in contrast to the beneficial role of ACEIs in cardiovascular disorders.  This work explored the potential effects of ramipril, an ACEI, compared to SVPA, on the behavior, and electrophysiology of the brain and heart in a rat model of status epilepticus. The dose dependent pattern of the presumed ramipril activities was investigated. Methods: Adult male rats were assigned into seven groups, controls, IP pyridostigmine (36 mg/kg)-induced status epilepticus (PISE), oral SVPA (5 mg/kg), and three groups receiving oral ramipril at respective doses of 5 (R5), 10 (R10), and 20 mg/kg (R20). Rat behavior was assessed using Racine’s motor convulsion scoring for 10 minutes.  Blood pressure was recorded, and electroencephalography (EEG) and electrocardiography (ECG) were performed on the sedated rats 24 hours after recovery. Results: Despite the partial behavioral improvement of motor convulsions with R5 and R10 exhibited epileptogenic activity, as indicated by the increased relative power of fast and slow gamma waves and total EEG power. R10 triggered arrhythmia and cardiac ischemia as indicated by absence of P wave, along with ST elevation and tall T wave, slowed heart rate and prolonged QRS, QTc, and RR intervals. Conclusion: PISE was resistant to sodium valproate and ramipril. Ramipril at low and moderate doses induced epileptogenic activity and, especially at moderate dose, precipitated cardiac ischemia and arrhythmia. SummaryThe debatable role of ramipril in epilepsy was studied in a rat model of pyridostigmine-induced status epilepticus, compared to sodium valproate. Increasing ramipril doses did not resolve status epilepticus in rats. Instead, low and moderate doses exhibited epileptogenic activity, opposite to high dose ramipril and sodium valproate. Blood pressure was dose-dependently reduced with ramipril. Electrocardiography showed evidence of cardiac arrythmia and ischemia, especially with the moderate ramipril dose. The behavioral and EEG indices correlated with systolic blood pressure and ECG changes.