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PubMed1992

[Ventricular repolarization].

Ventricular repolarisation is the period that depolarised cells require to become polarised, that is to say excitable. In general cardiological practice, the duration of repolarisation is assessed by measuring the QT interval on the surface electrocardiogram. This measurement may be difficult because of the lack of precision in defining the end of the T wave. Automatic systems are becoming available and should circumvent these difficulties of manual measurements. Interpretation of a change in the QT interval during drug administration or related to cardiac pathology should take the many sources of physiological variation of ventricular repolarisation into account. One of the main causes of this variation is the heart rate which influences the duration of repolarisation in a complex manner. Analysis of the duration of repolarisation has many implications in pathology and pharmacology. Prolongation of the QT interval and its failure to adapt to the heart rate are trigger factors for torsades de pointe. Many drugs prolonging the duration of repolarisation and of the ventricular refractory period are being developed. Their effects are partially dependent on the heart rate. Finally, prolongation of the QT interval is associated with a poor prognosis after myocardial infarction.

Action Potentials↗
PubMed2004

Key anatomic data for the use of rat heart in electrophysiological studies of the intracardiac nervous system.

The aim of the present study was to elucidate both the topography and architecture of the rat intrinsic cardiac nerve plexus, as this species becomes a frequent mammalian model for electrophysiological investigations of the intracardiac nervous system. Fifteen adult rats were examined employing histochemistry for acetylcholinesterase to visualize the intracardiac nerve plexus in hearts. Extracardiac nerves entering the rat heart were found amid aorta and pulmonary trunk as well as along both right and left cranial veins. The nerves from the arterial part of the heart hilum extended directly to the ventricles but the nerves from the venous part of the hilum interconnected among themselves forming a nerve plexus of the cardiac hilum on the heart base. Within the rat epicardium, intrinsic nerves clustered into six routes by which they selectively projected to different rat heart regions. Ventral wall of the ventricles was supplied by three neural subplexuses, dorsal ventricular wall--by one subplexus; each atrium received nerves from two distinct subplexuses. In conclusion, this morphological study demonstrates that rat intracardiac nerve plexus compounds to anatomical scheme of the same plexus in human, therefore rat is a usable model for electrophysiological experiments of the intracardiac nervous system.

Acetylcholinesterase↗
PubMed2005

[Effect of the metabolic syndrome on the electrophysiological parameters of the heart].

The goal of this research was to study influence of the MS on the electrophysiological parameters of the heart conduction system. The research involved 32 patients suffering from heart arrhythmias (18 females and 14 males, average age 52,8-/+12,9). The patients were categorized into 2 groups. Group I included 15 patients (9 females and 6 males, average age 47,5-/+8,9) suffering from heart arrhythmias and with signs of MS. Group I was subdivided into 2 subgroups: I subgroup--10 patients without diabetes, and II subgroup 5 patients with type II diabetes. Group II comprised of 17 patients (8 females and 9 males, average age 57,4-/+11,9) with arrhythmias without any signs of MS. The refractoriness dispersion between the right atrium (RA) and the left atrium (LA) caused by the MS, directly provokes development of atrial fibrillation and type II (atypical) atrial flutter. In cases of metabolic syndrome and "slow-fast" type of PRAVNT caused by the metabolic failures, the prolongation of the antegrade effective refractory period (ERP) of the slow AV nodal pathways and the retrograde ERP of the fast AV nodal pathways provoked prolongation of the tachycardia cycle and, consequently, reduction of the heart rate during paroxysms of tachycardia. Metabolic failures produce direct effect upon the sinus node function, causing suppression of its function as the SNSS develops, which requires implantation of pacemaker. The research results for metabolic syndrome and AV blockage cases demonstrated that the latter was always of a distal type, which was caused by a direct effect of metabolic failures upon the electrophysiology of the atrioventricular junction.

Adult↗