@article{HerbertSchmidt1992,
  author    = {Herbert, M. K. and Schmidt, R. F.},
  title     = {Activation of normal and inflamed fine articular afferent units by serotonin},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59952},
  year      = {1992},
  abstract  = {In cats anesthetized with alpha-chloralose, extracellular recordings were made from fine afferent units belonging to the medial articular nerve (MAN) of the knee joint. The excitatory and sensitizing effects on articular afferents of serotonin (5-HT) applied intra-arterially close to the joint were examined. The joints were either normal or an experimental arthritis had been induced some hours before the recording session. Bolus injections of 1.35-135 p,g 5-HT excited about 43\% of group 111 (CV: 2.5-20 m/sec) and 73\% of group IV units (CV: < 2.5 mjsec) from normal joints. The latency was usually between 10 and 30 sec, and the duration and size of the responses were dose-dependent. Fast group 111 units (CV: > 16 mjsec) and group li units (CV: > 20 m/sec) were never excited by 5-HT. Repetitiveadministration led to pronounced tachyphylaxis of the 5-HT response. Inflammation induced an enhanced sensitivity of group III articular afferent units to close intra-arterial application of 5-HT. In particular the total duration of each response was considerably prolonged (4-10 min against 1-2 min under normal conditions). At the same time the tachyphylaxis seen under normal conditions was gteatly reduced. In contrast, group IV articular afferent units did not become sensitized to 5-HT in the course of inflammation. In normal joints 5-HT did not sensitize fineafferent units for movement-induced responses. However, after inflammation, a distinct sensitization to such movements by 5-HT application could be observed bothin group 111 and group IV fiber ranges. The sensitization had a short time course not exceeding 7 min. The tonic component of the movement-induced response was more enhanced than the phasic one. The bolus application of 5-HT led to temporary vasoconstriction of the knee joint vessels. This vasoconstriction was especially pronounced in inflamed joints and impeded the access of subsequently applied substances to the terminal regions of the afferent units under observation. lt is concluded that the present results support the notion that 5-HT may participate in the mediation of pain from inflamed tissue such as an arthritic joint by exciting and sensitizing fine afferent units. During inflammation group 111 units are particularly sensitive to 5-HT and, thus, may carry the bulk of the 5-HT-induced nociceptive messages.},
  subject      = {Medizin},
  language  = {en}
}
@article{HerbertTaflerSchmidtetal.1993,
  author    = {Herbert, M. K. and Tafler, R. and Schmidt, R. F. and Weis, K. H.},
  title     = {Cyclooxygenase inhibitors acetylsalicylic acid and indomethacin do not affect capsaicin-induced neurogenic inflammation in human skin},
  series = {Agents Actions},
  volume    = {38},
  journal   = {Agents Actions},
  number    = {Special Conference Issue},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127666},
  pages     = {C25-27},
  year      = {1993},
  abstract  = {Neurogenic inflammation is evoked by neuropeptides released from primary afferent terminals and, presumably, by other secondarily released inflammatory mediators. This study examines whether prostaglandins might participate in the development of neurogenic inflammation in humans and whether cyclooxygenase inhibitors have any anti-inflammatory effect on this type of inflammation. In healthy volunteers, neurogenic inflammation was elicited by epicutaneously applied capsaicin (1 \%), after systemic pretreatment with acetylsalicylic acid, or topically applied indomethacin compared to pretreatment with saline or vehicle, respectively. The extent of neurogenic inflammation was quantified by planimetry of visible flare size and recording the increase of superficial cutaneous blood flow (SCBF) with a laser Doppler flowmeter. Capsaicin-induced flare sizes and outside SCBF (both representing neurogenically evoked inflammation) were unaffected by acetylsalicylic acid or indomethacin. Only the capsaicin-induced increase; of inside SCBF was attenuated by local pretreatment with indomethacin, reflecting the participation of prostaglandins in the inflammatory response of those areas which were in direct contact with capsaicin.},
  language  = {en}
}
@article{HerbertHolzer1994,
  author    = {Herbert, M. K. and Holzer, P.},
  title     = {Interleukin-1ß enhances capsaicin-induced neurogenic vasodilatation in the rat skin},
  series = {British Journal of Pharmacology},
  volume    = {111},
  journal   = {British Journal of Pharmacology},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-128171},
  pages     = {681-686},
  year      = {1994},
  abstract  = {No abstract available.},
  language  = {en}
}
@article{HerbertHolzer1994,
  author    = {Herbert, M. K. and Holzer, P.},
  title     = {Nitric oxide mediates the amplification by interleukin-1β of neurogenic vasodilatation in the rat skin},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59969},
  year      = {1994},
  abstract  = {No abstract available.},
  subject      = {Medizin},
  language  = {en}
}
@article{TaflerHerbertSchmidtetal.1993,
  author    = {Tafler, R. and Herbert, M. K. and Schmidt, R. F. and Weis, K. H.},
  title     = {Small reduction of capsaicin-induced neurogenic inflammation in human forearm skin by the glucocorticoid prednicarbate},
  series = {Agents Actions},
  volume    = {38},
  journal   = {Agents Actions},
  number    = {Special Conference Issue},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127698},
  pages     = {C31-34},
  year      = {1993},
  abstract  = {No abstract available.},
  language  = {en}
}