FE 200665 is a peripherally selective kappa-agonist with potent analgesic and antiinflammatory properties that may lead to improved analgesic-antiinflammatory therapy compared with centrally acting opioids or standard nonsteroidal antiinflammatory drugs.

These findings suggest an interplay of central and peripheral mechanisms of pain control. An effective central inhibition of pain apparently signals a reduced need for recruitment of opioid-containing immune cells to injured sites.

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The widespread use of neuraxial anaesthesia increases the need for animal models to evaluate therapeutic prospects, mechanisms and risks of this technique. As a methodological prerequisite, we characterised the sympathetic blockade after different modes of neuraxial anaesthesia with regard to segments supplying the splanchnic region. Under haemodynamic monitoring, lidocaine 2% or saline were infused via intrathecal (10 µl), lumbar epidural (10 and 30 µl) or thoracic epidural (10 and 30 µl) catheters. Segmental spread of neuraxially infused local anaesthetic was assessed using methylene blue. Mean arterial blood pressure decreased more severely after neuraxial lidocaine in thoracic epidural (10 and 30 µl) compared to high-volume (30 µl) lumbar anaesthesia animals. Determination of the sympathetic blockade by means of laser Doppler perfusion imaging was restricted to the paws due to a higher density of subcutaneous blood vessels as compared to the abdominal wall (mean ± SD: 3.93 ± 0.06 vs. 1.35 ± 0.05/384 mm², p < 0.05). Only high-volume (30 µl) lumbar and thoracic epidural anaesthesia (10 and 30 µl) increased skin perfusion in both hind and front paws. This extensive sympathetic blockade was demonstrated to include splanchnic segments using thermography. Segmental spread of methylene blue did not closely correspond to laser Doppler findings and should be interpreted as minimum rather than exact epidural spread of local anaesthetic.

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