Neuroendocrine pathway involvement in the loss of the cutaneous pressure‐induced vasodilatation during acute pain in rats

Abstract

Pain is regarded as a risk factor in pressure ulcer development by contributing to immobility. Pressure-induced vasodilatation (PIV) is a mechanism whereby cutaneous blood flow increases in response to progressive locally applied pressure, thereby delaying the occurrence of ischaemia and appearing to be a protective response to local pressure. When the interaction between nervous and vascular systems is deregulated, PIV, which relies on both systems, is absent. We thus hypothesized that acute pain could alter PIV. This study investigated the effects on PIV of acute pain triggered by noxious heat (50• C) applied to the tail of anaesthetized rats. To address the mechanisms underlying these effects, chronic sympathectomy was performed using guanethidine, and the plasma concentrations of pituitary adrenocorticotrophin (ACTH) and catecholamines were measured. Our results show that acute pain induces a loss of PIV associated with an increase of ACTH. Direct involvement of hypertensive effects and peripheral sympathetic nervous system are excluded in the loss of PIV, whereas the activation of brain structures that have descending inhibitory control cannot be excluded. A low dose of systemic morphine prevented this loss of PIV and maintained the ability of the cutaneous microcirculation to adapt to the applied pressure. The loss of a protective response to local pressure (PIV) induced by acute pain lends physiological support to the direct involvement of pain in pressure ulcer development. Therefore, an adequate evaluation and treatment of pain is crucial.

Endothelium‐derived hyperpolarizing factor as an in vivo back‐up mechanism in the cutaneous microcirculation in old mice

“…Indeed the different treatments had similar effects on changes in ABP in young adult and old mice, reflecting an absence of NO and PG functional loss in the general systemic circulation with ageing. We reported previously that an acute increase in ABP resulting from noradrenaline infusion did not abolish PIV in rats (Fromy et al 2007), suggesting that systemic cardiovascular effects of different treatments are unlikely to explain the loss of PIV in the present study.…”

Chronic sciatic nerve injury impairs the local cutaneous neurovascular interaction in rats

“…In contrast, PIV was not reduced on a cutaneous area not innervated by nerve injury (the side contralateral to the CNC) in short-term CNC rats (data not shown). These observations also suggest that in our experimental conditions, CNC did not activate nociceptive inputs to trigger the nociceptive signaling pathway to abolish PIV in healthy rats [13]. Thus, PIV reduction on a cutaneous area innervated by injured nerve was due to direct effect of the compression rather than nociceptive mechanisms.…”