TY - JOUR
T1 - Assessment of cardiac sympathetic regulation by respiratory-related arterial pressure variability in the rat
AU - Yang, Cheryl C.H.
AU - Kuo, Terry B.J.
PY - 1999/3/15
Y1 - 1999/3/15
N2 - 1. Mechanical ventilation evokes a corresponding arterial pressure variability (APV) which is decreased by β-adrenoceptor antagonism. Therefore, in this study we set out to determine whether the respiratory-related APV can be used to assess cardiac sympathetic tone. 2. Computer-generated broad-band mechanical ventilation (0-3 Hz) was applied to Sprague-Dawley rats that had been anaesthetized with ketamine and paralysed with pancuronium. APV and its relationship to lung volume variability (LVV-APV) was systematically quantified, with auto- or cross-spectral frequency domain analysis. 3. APV and LVV-APV transfer magnitudes between 0.5 and 1.5 Hz showed dose-dependent suppression by propranolol from 0.01 to 1 mg kg-1, while the static value of arterial pressure remained unchanged. Stroke volume variability, assessed by the use of a pulse contour method, exhibited a similar pattern of suppression by propranolol. In contrast, heart rate variability was not lowered with propranolol. 4. The effect of propranolol on respiratory-related APV persisted even in the presence of combined α-adrenoceptor and muscarinic receptor blockade by phentolamine and atropine. 5. The frequency range of 0.5-1.0 Hz was optimal for LVV-APV transfer magnitude to correlate with cardiac sympathetic tone. 6. We conclude that respiratory-related APV may provide a valid assessment of cardiac sympathetic regulation which is independent of parasympathetic and vascular sympathetic influences in ketamine-anaesthetized and positive pressure-ventilated rats.
AB - 1. Mechanical ventilation evokes a corresponding arterial pressure variability (APV) which is decreased by β-adrenoceptor antagonism. Therefore, in this study we set out to determine whether the respiratory-related APV can be used to assess cardiac sympathetic tone. 2. Computer-generated broad-band mechanical ventilation (0-3 Hz) was applied to Sprague-Dawley rats that had been anaesthetized with ketamine and paralysed with pancuronium. APV and its relationship to lung volume variability (LVV-APV) was systematically quantified, with auto- or cross-spectral frequency domain analysis. 3. APV and LVV-APV transfer magnitudes between 0.5 and 1.5 Hz showed dose-dependent suppression by propranolol from 0.01 to 1 mg kg-1, while the static value of arterial pressure remained unchanged. Stroke volume variability, assessed by the use of a pulse contour method, exhibited a similar pattern of suppression by propranolol. In contrast, heart rate variability was not lowered with propranolol. 4. The effect of propranolol on respiratory-related APV persisted even in the presence of combined α-adrenoceptor and muscarinic receptor blockade by phentolamine and atropine. 5. The frequency range of 0.5-1.0 Hz was optimal for LVV-APV transfer magnitude to correlate with cardiac sympathetic tone. 6. We conclude that respiratory-related APV may provide a valid assessment of cardiac sympathetic regulation which is independent of parasympathetic and vascular sympathetic influences in ketamine-anaesthetized and positive pressure-ventilated rats.
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U2 - 10.1111/j.1469-7793.1999.887ab.x
DO - 10.1111/j.1469-7793.1999.887ab.x
M3 - Article
C2 - 10066913
AN - SCOPUS:0033559377
SN - 0022-3751
VL - 515
SP - 887
EP - 896
JO - Journal of Physiology
JF - Journal of Physiology
IS - 3
ER -