Nurses need to understand how the body processes and modifies pain to provide optimal care for patients in pain. Previous work from our lab has shown that stimulation of the lateral hypothalamus (LH) produces analgesia in acute, non-inflammatory pain, but chronic pain changes the way the body responds to painful stimuli. To investigate the role of the LH in more prolonged pain, we measured foot withdrawal latencies (FWL) in female Sprague-Dawley rats using an inflammatory pain model. For the induction of inflammatory pain, the rats were lightly anesthetized with sodium pentobarbital, and mustard oil (20 µl) was applied on the left ankle. Either carbachol (125 nmol/0.05 µl normal saline) or normal saline for control was microinjected into the left LH, and response latencies measured. Mustard oil increased pain responses (hyperalgesia) compared to controls (1.92 ± 0.36 vs. 2.96 ± 0.30 sec, respectively, p < 0.05) that was reversed by LH stimulation to the level of controls (p>0.05). These data suggest that the LH is a part of a descending inhibitory pathway for inflammatory pain.
This work was supported by USPHS grants HHS NR04778 from the National Institute of Nursing Research at the National Institutes of Health.
Session #1199 - Pain
The 29th Annual MNRS Research Conference (April 1-4, 2005)