Autonomic and ventilatory components of heart rate and blood pressure variability in freely behaving rats

Abstract

The relative role of parasympathetic, sympathetic, and ventilatory influences in the genesis of blood pressure and R-R interval variability is controversial. In 13 freely behaving WKY rats instrumented with venous and arterial catheters and chest electrodes, mean arterial pressure (MAP, mmHg), R-R interval (ms), and respiratory fluctuations were monitored for 90 min in the control condition and after intravenous atropine (0.75 mg/kg) and/or propranolol (1 mg/kg). Spectral power (pw) in the 0.25- to 0.75-Hz (midfrequency, MF) and the 0.75- to 3.0-Hz (high-frequency, HF, respiratory-synchronous) bands was computed in sequences of 400 heartbeats by use of a combined autoregressive analysis. Atropine reduced but did not abolish HF R-R interval pw (from 1.73 +/- 0.50 to 0.39 +/- 0.27 ms2, P < 0.01) and halved HF MAP pw (from 0.41 +/- 0.30 to 0.21 +/- 0.12 mmHg2, P < 0.05), whereas propranolol did not affect HF pw of the R-R interval or MAP. Propranolol also failed to significantly modify MF R-R interval pw (from 0.48 +/- 0.44 to 0.40 +/- 0.34 ms2, P = NS) or MF MAP pw (from 0.54 +/- 0.39 to 0.42 +/- 0.20 mmHg2, P = NS), whereas atropine virtually abolished MF R-R interval pw (from 0.48 +/- 0.44 to 0.01 +/- 0.01 ms2, P < 0.01) and also significantly reduced MF MAP pw (from 0.54 +/- 0.39 to 0.33 +/- 0.24 mmHg2, P < 0.01). The effects of combined blockade were similar to those of atropine alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart rate variability as an index of physiological strain in hyperthermic and dehydrated rats

“…Results using HRV are consistent with earlier work with pharmacological blockade (Casadei et al, 1995;Cerutti et al, 1991;Perlini et al, 1995), but spectral analysis has the added advantage of no possible confusion of the results by neurological compensation for the removal of either the PNS or SNS branches of the autonomic nervous system.…”

“…In rats, the definitions of HF (0.75-3 Hz), mid-frequency (MF, equivalent to LF in humans, 0.25-0.75 Hz) and LF (equivalent to VLF in humans, 0.02-0.25 Hz) differ from that of humans only in frequency bands due to the higher heart and respiratory rates of rats. Very similar results were obtained in analogous bands on intravenous administration of atropine (parasympathetic blocker) and propranolol (sympathetic blocker) to rats (Cerutti et al, 1991;Perlini et al, 1995) as in humans (Pomeranz et al, 1985). Also as with humans, HRV in rats is due to autonomic and nonautonomic etiologies.…”

“…The central frequency of the high frequency (HF) peak of the HRV spectrum is identical to the peak generated by measuring respiration alone thus verifying that respiratory rhythm is directly associated with the HF peak (Perlini et al, 1995). The low frequency (LF) peak is associated with vasomotor tone linked to BP maintenance as demonstrated by the change in this portion of this peak associated with the BP changes seen on tilting or standing in humans (Lipsitz et al, 1990).…”

“…However, this increase is not reflected in increases in LF, MF, or HF area during heat stress. Since changes in these bands have been associated with changes in autonomic nervous system activity (Cerutti et al, 1991;Nelskla et al, 1999;Perlini et al, 1995), the increases in NSD during heating may be attributed to non-neuronal causes. However, diminished total HRV can result from both autonomic withdrawal and excessively high levels of autonomic input (saturation) (Task Force, 1996).…”

Chronic fluoxetine reduces autonomic control of cardiac rhythms in rats with congestive heart failure

“…The amplitude of the oscillations (and thus absolute power) in the LF domain depends, in part, on the underlying sympathetic tone that is modulated by the baroreflex. High-frequency (HF) oscillations are due primarily to respiratory-dependent effects on the parasympathetic control of HR and, to a lesser extent, to stretch of sinoatrial node cells during ventilation (34,39). In heart failure, loss of HRV is indicative of decreased cardiac vagal drive and an inability of the parasympathetic system to properly buffer elevated cardiac sympathetic drive, which contributes to ventricular arrhythmogenesis in CHF (42).…”