Chronobiological Aspects of the Heart Rhythm Disorders at the Change of Pulmonary Ventilation in Rat Model

Abstract

Presently is well established, that most physiological functions of living organisms fluctuate with a circadian dependence. Many experimental and clinical studies have demonstrated that cardiovascular functions show a marked circadian rhythmicity (Smith et al., 1987; Henry et al., 1990). Circadian fluctuations occur both in blood pressure and heart rate, but also in the ocurrence of ventricular dysrhythmias, the onset of cardiovascular symptoms, and the manifestations of cardiovascular diseases. Ventricular fibrillation is the most dangerous type of arrhythmia in humans and belongs to the group of the most frequent causes of sudden death after myocardial infarction. The development of ventricular fibrillation is strengthened by the difference between the duration of the refractory period and irregular electrical activity in the various parts of the heart. The probability of the development of such irregular activity is increased by an increased resting excitability, a decreased conduction velocity, and an increase in automaticity (Fisch, 1973; Opie et al., 1979; Carmeliet, 1988). The resistance of the heart to these disorders is dependent on its electrical stability, which can be measured by several parameters such as the duration of the vulnerable period (Wegria et al., 1941; Axelrod et al., 1975), ventricular flutter threshold (Szekeres & Papp, 1967), excitability threshold (Jones & Klein, 1982), or ventricular fibrillation threshold (Wegria et al., 1941; Gerst et al., 1966). Factors that contribute to the development of various cardiac disorders not only include local myocardial ischemia (Ferrier et al., 1985; Saint et al., 1992), but also hypoxia (Nishimura et al., 1989) and respiratory and metabolic acidosis (Gerst et al., 1966; Rogers et al., 1973; Kujanik et al., 1984; 1985). It is generally accepted that some disorders of pulmonary ventilation belong to the group of proarrhythmogenic factors. The effect of systemic hypoxia, hypercapnia and acidosis (consequences of hypoventilation or an apneic episode) were investigated not only in experimental studies (Kujanik et al., 1984; 1985, Tomori et al., 1997; 2000) but also in clinical ones (Guilleminault et al., 1983; Peter, 1990; Kujanik et al., 2000a; 2000b).