Neural mechanisms in the cardiovascular responses to acute central hypovolaemia

Roger G. Evans*, Sabatino Ventura, Roger Al Dampney, John Ludbrook

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

79 Citations (Scopus)

Abstract

1. The haemodynamic response to acute central hypovolaemia consists of two phases. During phase I, arterial pressure is well maintained in the face of falling cardiac output (CO) by-baroreceptor-mediated reflex vasoconstriction and cardio-acceleration. Phase II commences once CO has fallen to a critical level of 50-60% of its resting value, equivalent to loss of approximately 30% of blood volume. 2. During phase II, sympathetic vasoconstrictor and cardiac drive fall abruptly and cardiac vagal drive increases. In humans, this response is invariably associated with fainting and has been termed vasovagal syncope. 3. In both experimental animals and in humans, the responses to acute central hypovolaemia are greatly affected by anaesthetic agents, in that the compensatory responses during phase I (e.g. halothane) or their failure during phase II (e.g. alfentanil) are blunted or abolished. 4. Therefore, our present knowledge of the neurochemical basis of the response to hypovolaemia depends chiefly on the results of experiments in conscious animals. Use of techniques for simulating haemorrhage has greatly enhanced this research effort, by allowing the effects of multiple treatments on the response to acute central hypovolaemia to be tested in the same animal. 5. The results of such experiments indicate that phase II of the response to hypovolaemia is triggered, at least in part, by a signal from cardiac vagal afferents. There is also strong evidence that phase II depends on brainstem δ 1-opioid receptor and nitrergic mechanisms and can potentially be modulated by circulating or neuronally released adrenocorticotropic hormone, brainstem serotonergic pathways operating through 5-HT 1A receptors and opioids acting through μ- and κ-opioid receptors in the brainstem. 6. Phase II also appears to require input from supra-medullary brain centres. Future studies should determine how these neurotransmitter systems interact and their precise neuroanatomical arrangements.

Original languageEnglish
Pages (from-to)479-487
Number of pages9
JournalClinical and Experimental Pharmacology and Physiology
Volume28
Issue number5-6
DOIs
Publication statusPublished - 2001
Externally publishedYes

Keywords

  • Adrenocorticotropic hormone
  • Anaesthesia
  • Baroreceptors
  • Brainstem
  • Haemorrhage
  • Hypovolaemia
  • Nitric oxide
  • Opioids
  • Serotonin
  • Syncope

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