RESUMO
Hyperkalemia is a common electrolyte abnormality frequently complicated with chronic kidney disease. By injecting potassium chloride (KCl) solutions intravenously into bullfrogs, we reproduced typical electrocardiogram (ECG) abnormalities of hyperkalemia in the frog hearts, such as the peaked T waves and the widening of QRS complexes. Simultaneous recordings of cardiac action potentials showed morphological changes that synchronized with those of ECG. After 100 mM KCl injection, the widened QRS complexes continued for a while and gradually restored to their baseline widths. However, pre-treatment with sodium bicarbonate or salbutamol, which directly or indirectly stimulates Na+/K+-ATPase activity, significantly facilitated the recovery from the widened QRS duration, indicating the transcellular movement of potassium ions from the extracellular fluid into the intracellular stores.
Assuntos
Hiperpotassemia , Animais , Hiperpotassemia/induzido quimicamente , Hiperpotassemia/tratamento farmacológico , Hiperpotassemia/veterinária , Bicarbonato de Sódio/uso terapêutico , Rana catesbeiana , Albuterol/uso terapêutico , Potássio , Cloreto de Potássio , Eletrocardiografia/veterináriaRESUMO
Using bullfrog hearts, we previously reproduced a ST segment elevation in electrocardiogram (ECG), mimicking human ischemic heart disease. In the present study, by inducing subepicardial burn injuries on the inferior part of the frog heart ventricle, we could reproduce typical ECG changes observed in human inferior wall myocardial infarction, such as the marked elevation of the ST segments in inferior limb leads (II, III, aVF) and their reciprocal depression in the opposite limb leads (I, aVL). Due to the decrease in Na+/K+-ATPase protein expression, the resting membrane potential of injured cardiomyocytes shifted toward depolarization. Such induced electrical difference between the injured and intact cardiomyocytes was thought to be responsible for the creation of "currents of injury" and the subsequent ST segment changes.
Assuntos
Queimaduras , Infarto Miocárdico de Parede Inferior , Infarto do Miocárdio , Animais , Arritmias Cardíacas/veterinária , Queimaduras/veterinária , Eletrocardiografia/veterinária , Humanos , Infarto Miocárdico de Parede Inferior/veterinária , Infarto do Miocárdio/diagnóstico , Infarto do Miocárdio/veterinária , Miócitos Cardíacos , Rana catesbeianaRESUMO
Recent studies revealed the involvement of "chronic inflammation" in the pathogenesis of schizophrenia. In schizophrenia and some neurodegenerative disorders that are caused by inflammation, T-lymphocytes and macrophages were hyperactivated or proliferated in the central nervous system, being accompanied by the overexpression of delayed rectifier K+-channels (Kv1.3) within the cells. In our previous basic studies, in addition to nonsteroidal anti-inflammatory drugs (NSAIDs) and statins, antibiotics (clarithromycin, chloroquine), anti-hypertensive drugs (nifedipine, benidipine, diltiazem, verapamil) and anti-allergic drugs (cetirizine, fexofenadine, azelastine, terfenadine) strongly suppressed the Kv1.3-channel activity and pro-inflammatory cytokine production from lymphocytes. Given such pharmacological properties of these commonly used drugs, they may be useful in the treatment of schizophrenia, in which the enhanced cellular immunity and the subsequent release of excessive cytokines are responsible for the pathogenesis.