Gabapentin Prevents Delayed and Long-lasting Hyperalgesia Induced by Fentanyl in Rats

Abstract

Intraperitoneal and intrathecal gabapentin prevents the development of hyperalgesia induced by acute systemic exposure to opioids. This prevention may result, at least in part, from binding of gabapentin to the alpha2delta auxiliary subunits of voltage-gated calcium channels.

Role of gabapentin in preventing fentanyl- and morphine-withdrawal-induced hyperalgesia in rats

“…Dirks et al [14] found gabapentin significantly reduces postoperative morphine consumption after high-dose remifentanil-based anesthesia and suggested gabapentin as a preemptive antihyperalgesic for opioid-withdrawal hyperalgesia. Van Elstraete [15] first reported that gabapentin prevents the development of hyperalgesia induced by systemic exposure to fentanyl. However, few researchers have investigated the effect of gabapentin on both fentanyl-and morphine-withdrawalinduced hyperalgesia.…”

Neuropathic Pain Management in Chronic Laminitis

“…123 Laboratory animal data suggest the α 2 δ-ligands also have activity against opioid-induced hyperalgesia. 124 Documented therapeutic use in horses refers only to oral (PO) administration of gabapentin (Neurontin ® ) in two animals which were thought to exhibit signs of neuropathic pain, one in conjunction with acute femoral nerve injury post-surgery and one with a history of white line disease and chronic laminitis. 35,125 Lacking information on pharmacokinetic properties of the drug in the equine at that time, gabapentin doses were extrapolated from use in other species (2.5 mg/kg at intervals of 8, 12 or 24 hrs; 124 2.0-3.3 mg/kg at intervals of 8 or 12 hrs 35 ).…”

Beware of randomly used opioid!

“…comes from work using gabapentin , which has a presynaptic effect on glutamate release and dose dependently decrease OIH from repeat fentanyl in rats. 5 Modulation of spinal input by descending pathways from the brainstem is also implicated in the development of OIH, with a shift in the balance between descending inhibitory control towards pronociceptive system. These pronociceptive system may be more active in certain chronic pain states and also seems to play a role in OIH, acting via 5 HT 3 and possibly 5-HT 2 receptors.…”