1.
Bradykinin is considered to be an important mediator of
pain and
hyperalgesia associated with injury and
inflammation. Psychophysical studies were conducted in a patient with complete
kininogen deficiency to determine whether the absence of
bradykinin was associated with abnormalities in
pain sensibility.
Pain evoked by heat stimuli to the thenar eminence was tested before and after a localized
burn, which has been shown to cause
hyperalgesia in normal subjects. In addition,
pain evoked by intradermal administration of
bradykinin (0.1-10 micrograms) to the forearm and the effects of
bradykinin on
pain induced by heat stimuli were studied. The patient rated the intensity of
pain evoked by all heat stimuli relative to the
pain induced by a 3 s 45 degrees C stimulus. 2. The patient's heat pain threshold (45 degrees C) in the glabrous skin was similar to that of age-matched control subjects (n = 5) and to that previously observed in younger control subjects. 3. The
burn resulted in a decrease in pain threshold and an increase in
pain induced by suprathreshold stimuli. The magnitude of
hyperalgesia was within the range observed in the age-matched control subjects and in younger control subjects. Thus,
kinins are not essential for the development of
hyperalgesia after heat injury. 4. In control subjects,
intradermal injections of
bradykinin produced
pain and
hyperalgesia to heat stimuli. In the patient, intradermal
bradykinin injections induced minimal
pain and no
hyperalgesia to heat stimuli. Thus, congenital absence of
kininogens may be associated with a deficiency in
bradykinin receptors.