Circadian Rhythm of the Electrical Stability of the Rat Myocardium during Hyperventilation

Objective: Respiratory alkalosis is an extremely common and complicated problem affecting virtually every organ system of which the etiology may be associated with pulmonary or cardiovascular disorders. However, few studies have addressed the day/night rhythm of the effect of hyperventilation on the cardiovascular system. As such, the aim of the present study was to characterize the circadian rhythm of the electrical stability of the rat heart under hyperventilatory conditions.

Methods: Circadian rhythms of the electrical stability of the heart, measured according to ventricular arrhythmia threshold (VAT), were followed during normal artificial ventilation in a control group (respiratory rate, 40 breaths/min; tidal volume, 1 mL/100g [n=17]) and during hyperventilation (respiratory rate, 80 breaths/min; tidal volume 2 mL/100 g [n=7]) in female Wistar rats anesthetized with pentobarbital (40 mg/kg, administered intraperitoneally), after 4 weeks’ adaptation to a light (12 h)/dark (12 h) regimen (40%–60% humidity, temperature 24
C, 2 animals per cage with ad libitum access to food and water), with the dark period from 18:00 h to 06:00 h. Results are expressed as mean ± standard deviation. The basic circadian parameters were assessed using single and population mean cosinor tests.

Results: Under normoxic conditions, the 24 h course of VAT exhibited the highest susceptibility of the rat ventricular myocardium to arrhythmias between 12:00 h and 15:00 h, and the highest resistance between 19:20 h and 00:28 h (acrophase, -338° [in time at 22:53 h], with confidence intervals from -288
to -7
[19:20 h to 00:28 h]). The mean mesor (± SD) and amplitude were 2.59 ± 0.53 mA and 0.33 ± 0.11 mA, respectively. Nonsignificant hyperventilation increased the VAT at each interval of the measurement but did not alter the characteristics of circadian rhythm. Acrophase was on -40
(02:40 h), mesor was increased (2.91 mA), and amplitude was decreased (0.13 mA).

Conclusion: Although hyperventilation insignificantly increased the electrical stability of the heart compared with values during normal pulmonary ventilation during the entire 24-hour period, results demonstrated that hyperventilation probably only modulated-but did not disturb-the circadian rhythm of the electrical stability of the heart in pentobarbital-anaesthetized female Wistar rats. These results affirm that light/dark cycle-related differences are not merely transient or procedure dependent, but are a systematic response caused by distinct neurohumoral regulation during the light and dark periods of the day, and also occur under pentobarbital anesthesia.