The high-frequency component of the systemic arterial pressure spectrum is likely generated by respiratory pumping, while the lower-frequency end is amplified by the beta-adrenergic system.
Animal data on pressure variability mechanisms require human validation; leaves open effects of beta-blockade on SAP spectra in patients.
We evaluated the hypothesis that fluctuations in systemic arterial pressure (SAP) are under the influence of the respiratory pumping mechanism subjected to a modulatory action by the autonomic nervous system that is exerted primarily on the heart. Computer-generated broad-band mechanical ventilation (0-3 Hz) was applied to Sprague-Dawley rats that were anesthetized with ketamine and paralyzed with pancuronium. We observed excellent coherence between lung volume and SAP signals at ventilatory rates between 0.5 and 2.5 Hz; this coherence was unaffected by phentolamine, propranolol, atropine, bilateral vagotomy, or ventilatory stroke volume at 2-4 ml. Whereas bilateral vagotomy exerted no discernible effect, propranolol elicited a significant frequency-dependent (0.5-1.5 Hz) reduction in the magnitude of lung volume-SAP and lung volume-pulse pressure transfer functions. There was also a shift toward 0 degree for the phase of the lung volume-SAP transfer function over the same frequency range. We conclude that the high-frequency component (0.8-2.4 Hz) of the SAP spectrum may be generated by the respiratory pumping mechanism. However, the lower-frequency end of this mechanical influence is subjected to additional amplification by the autonomic nervous system, in which the beta-adrenergic system played a major role via its influence on the heart.
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Kuo et al. (1996) studied this question.
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