(1)
Department of Anaesthesia, Royal Free Hospital, London, UK
3.1 Peripheral Mechanisms
The activation of nociceptors depends on the magnitude of the stimuli. A stimulus larger than the threshold can alter subsequent receptor responses. This lowered threshold for pain manifests as hyperalgesia.
Lowered threshold to stimuli occurs at the site of trauma causing primary hyperalgesia. It may also manifest spontaneous pain. The surrounding area can become sensitised and manifest secondary hyperalgesia. This may manifest increased sensitivity to mechanical but not thermal stimuli. Both the areas exhibit increased responsiveness to decreased stimulus threshold and increased response to suprathreshold stimulus.
Primary hyperalgesia is contributed by many factors:
Direct stimulation of nociceptors: kinins (bradykinin, kallidin) can stimulate C and Aδ receptors. Stimulation is also seen by prostaglandins which are induced due to tissue injury. ATP desensitises receptors of the P2X family and causes pain. Capsaicin and protons are pain generators as well. Protons alter nociceptor physiology by altering Na, K and Ca channels. Capsaicin opens the cation permeable ion channel, initially causing the release of substance P and then leading to its depletion. Serotonin acts on 5HT3 receptors and sensitises ion channels. Norepinephrine increases the sensitivity of nociceptors via α1 and α2 receptors on the neuronal surface. This enhanced sensitivity is only seen in the presence of tissue injury.Related posts:
Full access? Get Clinical Tree
