Impact of pulse pressure on the respiratory-related arterial pressure variability and its autonomic control in the rat

Cheryl C.H. Yang, Terry B.J. Kuo

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

The autonomic control of respiratory-related arterial pressure variability (RAPV) remains uncharacterised. We set out to test the hypothesis that the autonomic nervous system may participate in RAPV via its effect on pulse pressure (PP). Experiments were performed on adult male Sprague-Dawley rats anaesthetised with ketamine and paralysed with pancuronium under positive-pressure ventilation. Respiratory variability in each parameter was quantified by auto-spectral analysis and the relationship between variabilities in two signals assessed by cross-spectral analysis. PP and systolic pressure (SP) exhibited similar powers of respiratory variability that were far more pronounced than for diastolic pressure (DP) or mean pressure (MP). The variability in PP preceded that in SP, MP or DR. The largest phase lag occurred between PP and DP and was equivalent to the time delay of one pulse interval. Coherence between respiratory variabilities in PP and MP was nearly perfect. Propranolol dose dependently suppressed respiratory variability in each pressure parameter and eventually disrupted the PP-MP relationship in respiratory variability. However, the influence of lung volume on MP persisted with a near-zero phase lag. Combined administration of phentolamine and atropine facilitated respiratory variability in PP and SP and failed to block the effect of propranolol. However, the combined administration moved the dose/response curve of propranolol and respiratory variability in each pressure parameter to the right. We conclude that, in addition to non-autonomic mechanisms, RAPV may be facilitated by cardiac sympathetic function via the effect on PP variability. The autonomic mechanism can still be evoked during combined α-adrenoceptor and muscarinic blockade, possibly via baroreflex mechanisms.

Original languageEnglish
Pages (from-to)772-780
Number of pages9
JournalPflugers Archiv European Journal of Physiology
Volume439
Issue number6
DOIs
Publication statusPublished - 2000
Externally publishedYes

Fingerprint

Rats
Arterial Pressure
Blood Pressure
Pressure
Propranolol
Pancuronium
Positive-Pressure Respiration
Baroreflex
Phentolamine
Autonomic Nervous System
Ketamine
Spectrum analysis
Atropine
Adrenergic Receptors
Cholinergic Agents
Sprague Dawley Rats
Lung
Neurology

Keywords

  • Autonomic nervous system
  • Blood pressure
  • Respiration

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Physiology (medical)

Cite this

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abstract = "The autonomic control of respiratory-related arterial pressure variability (RAPV) remains uncharacterised. We set out to test the hypothesis that the autonomic nervous system may participate in RAPV via its effect on pulse pressure (PP). Experiments were performed on adult male Sprague-Dawley rats anaesthetised with ketamine and paralysed with pancuronium under positive-pressure ventilation. Respiratory variability in each parameter was quantified by auto-spectral analysis and the relationship between variabilities in two signals assessed by cross-spectral analysis. PP and systolic pressure (SP) exhibited similar powers of respiratory variability that were far more pronounced than for diastolic pressure (DP) or mean pressure (MP). The variability in PP preceded that in SP, MP or DR. The largest phase lag occurred between PP and DP and was equivalent to the time delay of one pulse interval. Coherence between respiratory variabilities in PP and MP was nearly perfect. Propranolol dose dependently suppressed respiratory variability in each pressure parameter and eventually disrupted the PP-MP relationship in respiratory variability. However, the influence of lung volume on MP persisted with a near-zero phase lag. Combined administration of phentolamine and atropine facilitated respiratory variability in PP and SP and failed to block the effect of propranolol. However, the combined administration moved the dose/response curve of propranolol and respiratory variability in each pressure parameter to the right. We conclude that, in addition to non-autonomic mechanisms, RAPV may be facilitated by cardiac sympathetic function via the effect on PP variability. The autonomic mechanism can still be evoked during combined α-adrenoceptor and muscarinic blockade, possibly via baroreflex mechanisms.",
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