Related Experiment Videos
Sympathectomy does not abolish bradykinin-induced cutaneous hyperalgesia in man
Richard A Meyer1, Karen D Davis, Srinivasa N Raja
1Department of Neurosurgery, Johns Hopkins University, Baltimore, MD 21287-7713 USA Department of Anesthesiology, Johns Hopkins University, Baltimore, MD 21287-7713 USA Department of the Applied Physics Laboratory, Johns Hopkins University, Baltimore, MD 21287-7713 USA.
Abstract:
Bradykinin is an endogenous peptide that is thought to be a chemical mediator of the hyperalgesia following inflammation. In rat, bradykinin has been postulated to cause hyperalgesia to mechanical stimuli by releasing prostaglandin from sympathetic post-ganglionic terminals. The aim of this study was to determine whether bradykinin-induced cutaneous hyperalgesia in humans requires post-ganglionic sympathetic terminals. In humans, intradermal injection of bradykinin produces dramatic hyperalgesia to heat but not mechanical stimuli. Therefore, we measured the magnitude and duration of pain and hyperalgesia to heat stimuli following intradermal injection of bradykinin into the leg of a woman before and 6 months after an ipsilateral, surgical, lumbar sympathectomy. The pain and hyperalgesia to heat following bradykinin was found to be unaffected by the sympathectomy. These results suggest that the algesic effects of cutaneous bradykinin in human are independent of the sympathetic nervous system.