Key result
In conscious rabbits, acute stressors induced a reduction of vascular conductance in the facial artery ranging from 24% to 55%, which was abolished by phentolamine and delayed by decentralization.
Why the study?
Does acute stress activate the sympatho-adrenal axis as detected by haemodynamic recordings in conscious rabbits?
Does acute stress activate the sympatho-adrenal axis as detected by haemodynamic recordings in conscious rabbits?
In conscious rabbits, rapid release of adrenaline makes a prominent contribution to vasoconstriction in response to various acute stressors, highlighting the importance of the sympatho-adrenal axis.
Confirms sympatho-adrenal vasoconstriction in rabbit stress models; leaves open translation to human haemodynamics.
AIMS: When assessing sympathetic activation in acute stress, the attention is often limited to the sympatho-neural axis, whereas sympatho-adrenal activation, that can only be detected with poor time resolution from the concentration of plasma catecholamines, is often neglected. This study is aimed at re-investigating the role and the relevance of the sympatho-adrenal system in acute stress based on the analysis of haemodynamic responses in conscious rabbits. METHODS: Experiments were carried out on 19 rabbits implanted with chronic probes for arterial blood pressure and for blood flow in the facial artery. Cardiovascular responses to a randomized sequence of acute stressors (pinprick, air jet, oscillation of the cage, inhalation of formaldehyde vapours and im injection of hypertonic saline) were recorded before and after α-adrenergic blockade (phentolamine) and unilateral section of the cervical sympathetic trunk (decentralization). Plasma catecholamine concentrations were analysed in four animals. RESULTS: All stressors induced an increase in arterial blood pressure and a reduction of vascular conductance in the facial artery ranging on average from 24% (pinprick) to 55% (box oscillation). Such vasoconstrictor response was abolished by phentolamine. In decentralized arteries, the vasoconstriction was delayed by 10-15 s and decreased in magnitude in a stressor-dependent way, indicating an adrenaline-mediated effect in the late phase of the stress response that was confirmed by changes in plasma adrenaline concentration. CONCLUSIONS: In conscious rabbits, rapid release of adrenaline makes a prominent contribution to vasoconstriction in response to different stressors including box oscillation, muscle pain and air jet but not the nasopharyngeal stimulation.
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Roatta et al. (2010) studied Acute stress (n=19). Acute stressors before and after α-adrenergic blockade and unilateral section of the cervical sympathetic trunk vs. Baseline (before blockade/section) was evaluated on Arterial blood pressure and vascular conductance in the facial artery. In conscious rabbits, acute stressors induced a reduction of vascular conductance in the facial artery ranging from 24% to 55%, which was abolished by phentolamine and delayed by decentralization.
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