Intrathecal l-arginine reduces the antinociception of sevoflurane in formalin-induced pain in rats

Abstract

The purpose of this study was to investigate the contribution of spinal nitric oxide (NO) to the antinociceptive effects of emulsified sevoflurane in rats. Formalin tests were used to assess the nociceptive response. Immunohistochemistry was performed to determine the effects of emulsified sevoflurane on formalin-induced changes of Fos-like immunoreactive (Fos-LI)-positive neurons in the spinal cord. We found that emulsified sevoflurane administered intraperitoneally at a dosage of 2.5 ml/kg did not impair motor performance in rats, but it significantly decreased the formalin-induced paw licking time. Furthermore, Fos-LI-positive neurons were mainly found in the ipsilateral dorsal horn after the injection of formalin. The administration of emulsified sevoflurane significantly decreased Fos-LI-labeled neurons. Finally, intrathecal L-arginine alone did not affect the basal pain threshold, but it significantly decreased the antinociceptive response of emulsified sevoflurane against formalin injection and the suppressive effects of sevoflurane on formalin-induced Fos protein expression (P<0.05). These data suggest that spinal cord NO is involved in the antinociception of sevoflurane in rats.

Retracted: Effects of microRNA‐206 and its target gene IGF‐1 on sevoflurane‐induced activation of hippocampal astrocytes in aged rats through the PI3K/AKT/CREB signaling pathway

“…In addition, our results showed that thermal and mechanical thresholds of aged rats induced by sevoflurane decreased, and the cognitive functions were improved, indicating that miR‐206 could alleviate inflammatory pain through inactivation of astrocytes As an inhalation anesthetic, sevoflurane is widely applied in clinical settings, probably owing to its weak analgesic effect, which may reduce reaction to pain (Chen, Zeng, Dai, & Tang, ; DeSousa & Ali, ). MiR‐206 positively regulates the inflammatory response by targeting NR4A2 in human astrocytes (Duan et al, ).…”

Activation of peripheral group III metabotropic glutamate receptors suppressed formalin‐induced nociception

“…The abundance of FLI neurons was directly associated with the intensity of stimulation, and this has been used widely to examine the analgesic efficacy of therapeutic agents. 32,33 Peripheral administration of L-SOP significantly decreased FLI neurons in laminae I-II and V-VI of the ipsilateral spinal cord dorsal horn, suggesting that L-SOP produces antinociceptive effects in rat spinal cord.…”

“…29,30 To a certain extent, the numbers of FLI-positive neurons were directly associated with the stimulation intensity and have been used as markers of activation of nociceptive pathways. [31][32][33] Subcutaneous injection of formalin triggered FLI in the spinal cord. We observed a significant increase of FLI neurons that were found mainly in laminae I-II and V-VI of the dorsal horn belonging to formalin injection, 33 where nociceptive Aδ and C primary afferent fibres mainly terminated and spinal nociceptive signals were…”

Further analysis of acute antinociceptive and anti‐inflammatory actions of 4‐phenylselenyl‐7‐chloroquinoline in mice

“…Additionally, it is established that an increase in the production of NO will lead to an augmentation of the synthesis or release of pro‐inflammatory mediators, promoting inflammatory reactions and nociceptive sensations . There is evidence that the activation of NO synthase (NOS) with a consequent production of NO plays an important role in the central and peripheral modulation of nociception . On the other hand, experimental data have also demonstrated that NO inhibits nociception in the peripheral and also in the central nervous system.…”