The circadian rhythm of ventricular fibrillation threshold (VFT) and its relation to the heart rate (HR) and the rectal temperature (RT) was studied in female Wistar rats. The animals were exposed to daily light-dark cycles of 12 h of light alternating with 12 h of darkness and were under pentobarbital anaesthesia (40 mg/kg i.p.). The experiments were performed on open chest animals and VFT was measured by direct stimulation of the myocardium. VFT in female rats showed a circadian rhythm with the acrophase -338° (at 22.53 h), with the mesor 2.58 mA and the amplitude 0.33 mA. HR was not significantly changed during the experiments and no dependence was found between VFT and HR during the whole 24-hour period (r=0.08). The acrophase of the circadian rhythm of HR (on -47°, i.e. at 03.08 h) was shifted to the acrophase of VFT. The circadian rhythms of RT before the application of the anaesthetic agent and under general anaesthesia before the operative interventions had a very similar course with the nearly corresponding acrophoses as the circadian rhythm of VFT. It is concluded that the electrical stability of the rat heart measured by VFT shows the significant circadian rhythm in a parallel with the circadian rhythm of RT and probably without dependence on the changes of HR.
In 77 young healthy volunteers of both sexes the dependence of the QT interval of ECG on the heart rate was investigated during normal ventilation (control) and after 1, 2, 3, 4 min of voluntary hyperventilation, after 6 min of hypoxic-hypercapnic ventilation (through an enlarged dead space) and during the Valsalva manoeuvre. The absolute coefficients (a) of the regression lines QT = a + b . HR were significantly different in all groups. The slopes of regression lines (b) were significantly different in all groups with the exception of 4 min hyperventilation. Our results indicate that short-term alterations of pulmonary ventilation may change not only the duration of the QT interval but also its dependence on the heart rate. Voluntary hyperventilation lasting 1-2 min and the Valsalva manoeuvre decrease the rate dependence of the QT interval and this change may cause its prolongation at higher heart rates.
The aim of the study was to determine the dependence of changes in the electrical stability of the heart on the light-dark cycle (LD cycle) in disorders of pulmonary ventilation. The ventricular arrhythmia threshold (VAT) was measured in female Wistar rats (adaptation to the light regime 12:12 h, ketamine/xylazine anesthesia 100 mg/15 mg/kg, i.m., open
chest experiments). The conditions of the normal artificial ventilation and reoxygenation were VT = 1 ml/100 g, respiratory rate 40 breaths/min, hypoventilation VT = 0.5 ml/100 g, respiratory rate 20 breaths/min. The animals (n=11 light group; n=19 dark group) were subjected to 20 min hypoventilation followed by 20 min reoxygenation. The control
prehypoventilatory VAT differences were not found between the light (1.90
±0.84 mA) and dark (1.88±0.87 mA) part of the day. Artificial hypoventilation changed the VAT values in light and dark part of the day differently. While during the light period, the average VAT values in most animals (90.9 %) were significantly decreased (1.29±0.59 vs. 1.90±0.84 mA control, p<0.05), during the dark part these values showed either significant increase (63.2 %) (2.23±0.77 vs. 1.48±0.39 mA, p<0.005) or a slight non-significant decrease (36.8 %) (2.18±0.89 vs. 2.54±0.99 mA).
Reoxygenation returned the VAT values to the level before hypoventilation by an increase of the VAT (81.8 %) in the light part of day and by decrease of the VAT (68.4 %) in the dark part of the day. It is concluded that 1) in hypoventilation/reoxygenation model, the significant higher average VAT values are in the dark part of the day vs. the light one, 2) rat hearts are more resistant to systemic hypoxia and reoxygenation in the dark part of day, and 3) proarrhythmogenic effect of the systemic hypoxia is only seen in the light part of the day.
The Frank orthogonal corrected ECG and its first derivation were recorded in 27 healthy volunteers (women aged 19-22 years) during normal ventilation at rest (control group), after voluntary hyperventilation lasting 75 seconds, and during hypoxic-hypercapnic ventilation (through the enlarged dead space) lasting 5 min. The projections of the magnitude and direction of the positive and negative QRS derivation maxima into the horizontal, frontal, left sagittal planes and their spatial distribution were constructed. The magnitude of the positive and negative QRS derivation maxima was significantly decreased during hypoxic-hypercapnic ventilation. A significant alteration in the direction only arose at the positive maximum during hypoxic-hypercapnic ventilation in the frontal plane. The intrinsicoid deflection was not significantly altered. The normal values of the maxima of the first QRS derivation in young healthy women are given. It is supposed that the decrease in amplitude of the maxima of the first QRS derivation is caused by slowed propagation of the depolarization wave under hypoxic- hypercapnic conditions and alteration of the direction of the positive maximum is caused by a greater participation of the right ventricle at the origin of the resulting QRS vector.
The influence of some pulmonary ventilation alterations (the normal ventilation at rest = control), the hyperventilation (HV) lasting 75 s, the hypoxic-hypercapnic ventilation (HXV) lasting 3 and 6 min) on the instantaneous QRS vectors was investigated in 42 young healthy women (19-24 years old). The magnitude and the direction of instantaneous QRS vectors in the 10th to the 70th ms and in QRS max were constructed from the Frank lead ECG. The significant alterations of the direction (angle) were found in the 30th ms and QRS max at HXV and in the 60th ms at HV. A significant decrease in the magnitude of instantaneous vectors was found in the 10th to 50th ms after 6 min of HXV, in the 30th to 50th ms at 3 min of HXV, in the 40th to 50th ms at HV. These alterations were the most marked in the horizontal plane. We suggest that the alterations of the instantaneous QRS vectors were caused by the influence of the autonomic nervous system or humoral agents, but not by heart position, Brody’s effect or lung hyperinflation.