Analysis of the respiratory component of heart rate variability in the Cururu toad Rhinella schneideri

Figure 1. Representative traces showing raw electrocardiogram signal (ECG), the instantaneous RR interval (A) and the associated lung inflation cycles (buccal pressure cannula; B) in the cardiorespiratory interaction of one toad Rhinella schneideri during normoxia. High-speed traces show the ECG waveform (C) in pace with one lung inflation cycle (D).

Figure 2. Representative power spectrum of the RR interval and associated histogram for lung inflation cycles in one toad Rhinella schneideri during normoxia. Spectrum of the RR interval exhibits a less defined ventilatory-related peak that emerges in a more scattered range of frequencies (A). Lung inflation cycles presented as frequency distribution histograms binned into 0.001 Hz width band (B) for comparison purposes with the spectrum of the RR interval (Data represents animal from Fig. 1).

Figure 3. Waterfalls showing the spectra calculated under normoxia (A) and hypoxia (B) before and after selective autonomic blockade. Data sets consisting of 1,500 seconds were chosen within each condition: (A) Normoxia (N = 9); muscarinic blockade with atropine (N = 5); β-adrenergic blockade with sotalol (N = 4); and double autonomic blockade (DB; N = 9). (B) Hypoxia (FIO2: 0.05; N = 13); muscarinic blockade (N = 6); β-adrenergic blockade (N = 7); double autonomic blockade (DB; N = 13). Each spectrum was obtained following calculations of the average among all spectra of animals from the group at particular conditions. The standard error of the mean for the pooled data is omitted for clarity. For significant differences, see Table 1.

Figure 4. Cardiorespiratory interaction under hypoxia in the toad Rhinella schneideri. Waterfalls showing the spectra calculated (A) and associated histograms for lung inflation cycles (B) in one representative toad before and after selective autonomic blockade (atropine + sotalol) under hypoxic conditions (FIO2: 0.05). The respiratory-related peak in the heart rate variability was mostly abolished by the parasympathetic blockade (atropine). β-adrenergic after muscarinic blockade further diminished, but not eliminated, the remaining respiratory peak.

Figure 5. Representative recordings from one toad Rhinella schneideri (same as in Fig. 4) depicting raw electrocardiogram signals, the instantaneous RR interval and the associated lung inflation cycles (buccal pressure cannula) showing a cardiorespiratory interaction during hypoxia before (Ai and Bi), after muscarinic (Atropine; Aii and Bii) and double autonomic blockade (DB) (Aiii and Biii). Note that the amplitude oscillations in the RR interval associated with respiratory cycles were considerably diminished by the parasympathetic blockade (atropine).

Figure 6. Cardiorespiratory interaction under hypoxia in the toad Rhinella schneideri. Waterfalls showing the spectra calculated (A) and associated histograms for lung inflation cycles (B) in one representative toad before and after selective autonomic blockade (sotalol + atropine) under hypoxic conditions (FIO2: 0.05). In contrast to Fig. 4, the respiratory-related peak in the heart rate variability was mostly abolished by the sympathetic blockade (sotalol). Muscarinic after β-adrenergic blockade completely abolished the remaining respiratory peak.

Figure 7. Representative recordings from one toad Rhinella schneideri (same as in Fig. 6) depicting raw electrocardiogram signals, the instantaneous RR interval and the associated lung inflation cycles (buccal pressure cannula) showing a cardiorespiratory interaction during hypoxia before (Ai and Bi), after β-adrenergic (Sotalol; Aii and Bii) and double autonomic blockade (DB) (Aiii and Biii). Note that the amplitude oscillations in the RR interval associated with respiratory cycles were diminished by the sympathetic blockade (sotalol) and the remaining oscillation was totally removed by the parasympathetic drug (atropine).