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Spinal nitric oxide mediates antinociception from intravenous morphine
H K Song1, H L Pan, J C Eisenach
1Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1009, USA.
Anesthesiology
|July 17, 1998
Summary
Spinal nitric oxide (NO) plays a key role in pain relief from morphine. Inhibiting NO pathways reduces morphine
Area of Science:
- Neuroscience
- Pharmacology
- Pain Research
Background:
- Spinal nitric oxide (NO) is often considered pronociceptive.
- Morphine activates descending noradrenergic pathways and increases spinal NO synthesis.
Purpose of the Study:
- To investigate the role of spinal NO in morphine-induced pain relief.
Main Methods:
- Rats received intrathecal injections of various antagonists and inhibitors before intravenous morphine administration.
- Antinociception was measured by hind paw withdrawal latency from a heat source.
Main Results:
- Intravenous morphine produced dose-dependent antinociception.
- Spinal alpha2-adrenergic antagonists, NO synthase inhibitors, and NO scavengers attenuated morphine's pain-relieving effects.
Conclusions:
- Spinal NO mediates antinociception produced by intravenous morphine.
- This supports a spinal alpha2-adrenergic mechanism in morphine's pain relief.