Fascia iliaca compartment block: its efficacy in pain control for patients with proximal femoral fracture.

BACKGROUND: Proximal femoral fractures are common in elderly patients. Recently, use of regional blockade has gained popularity as a means of relieving pain among this patient population. Among the procedures, fascia iliaca compartment block (FICB) is believed to be advantageous because of its safety and efficacy. METHODS: In this study fifty-six consecutive patients who sustained a proximal femoral fracture were assigned to two groups. For 31 patients in group 1, FICB was used to control pre and postoperative pain. FICB was performed by an orthopaedic resident on arrival of the patient at the hospital and in the immediate postoperative period. Systemic administration of non-steroidal anti-inflammatory drugs (NSAIDs) alone was adopted for pain control for 25 patients in group 2. The severity of pain was assessed by use of a visual analog scale (VAS). RESULTS: Neither blockade-associated complications nor analgesic failure were encountered among patients who underwent FICB (group 1). In this group of patients, the mean preoperative VAS scores before FICB and at 10 min and 12 h after the blockade were 91, 31, and 36 respectively, indicating significant pain reduction. The corresponding values for group 2 patients were 92, 92, and 81. In addition, postoperative pain was also successfully managed by FICB with mean VAS scores at immediate, 6-h and 12-h time points of 15, 22, and 31 respectively, whereas the corresponding values for the group 2 patients were 62, 49, and 59. Consequently, significant differences in VAS scores were demonstrated between the groups in both the pre and postoperative periods. CONCLUSION: FICB is clinically safe and efficient, providing consistent analgesic effects irrespective of the performing doctor's experience of elderly patients with proximal femoral fracture.

Dopamine D2-like receptor in the nucleus accumbens is involved in the antinociceptive effect of nitrous oxide.

BACKGROUND: The mechanism of the antinociceptive effects of nitrous oxide (N(2)O) has not been completely elucidated. On the other hand, numerous studies have indicated that mesolimbic dopaminergic neurons, which are thought to be involved in rewarding and reinforcement processes, play important roles in the supraspinal pain-suppression system. We hypothesized that the mesolimbic dopaminergic system is involved in the antinociceptive effect of N(2)O. METHODS: Adult male Fischer rats were used in this study. To examine whether the dopaminergic system is activated by N(2)O, frozen sections of the ventral tegmental area of rats exposed to 75% N(2)O were double-stained for c-Fos and tyrosine hydroxylase. To clarify whether the dopaminergic system is involved in the antinociceptive action of N(2)O, saline or raclopride, a dopamine D(2)-like receptor antagonist, was injected into the nucleus accumbens (NAc) shell region. After exposure to 25% oxygen-75% nitrogen or 25% oxygen-75% N(2)O for 30 min, rats were subjected to formalin test, and the spinal cord was examined immunohistochemically. RESULTS: Exposure to 75% N(2)O increased c-Fos expression in tyrosine hydroxylase-positive cells in the ventral tegmental area. Raclopride, injected into the NAc shell region, attenuated the antinociceptive effect of N(2)O in the formalin test, and blocked the suppressive effect of N(2)O on the formalin-induced c-Fos expression in the dorsal horn of the spinal cord by N(2)O. CONCLUSION: It is possible that inhalation of N(2)O activates mesolimbic dopaminergic neurons, and that the antinociceptive effect of N(2)O is at least partially mediated by dopamine D(2)-like receptors in the NAc shell region.

Activity of the serotonergic system during isoflurane anesthesia.

BACKGROUND: Microdialysis studies have demonstrated that the release of serotonin (5-hydroxytryptamine, 5-HT) in the serotonergic projection areas increases during waking and decreases during sleep in rat and cat, suggesting that 5-HT plays an important role in modulation of sleep. Although it might be expected that 5-HT release is also decreased during general anesthesia, the functional contribution of serotonergic neurons in pharmacological effects of volatile anesthetics has not been fully investigated. METHODS: Using an in vivo microdialysis technique, we measured extracellular 5-HT in rat frontal cortex during waking, slow-wave sleep, and isoflurane anesthesia. To assess the involvement of the serotonergic system in the hypnotic action of isoflurane, the concentration of isoflurane required for loss of righting reflex was determined with or without pretreatment of fluoxetine hydrochloride, a selective 5-HT reuptake inhibitor. RESULTS: During slow-wave sleep and isoflurane anesthesia (0.1-1.5 MAC), 5-HT release decreased to 21%-44% of that during the waking state. Loss of righting reflex occurred at significantly higher isoflurane concentrations in fluoxetine-treated rats (0.76% +/- 0.03% [n = 8]) than in control rats (0.60% +/- 0.01% [n = 8]). CONCLUSIONS: It is suggested that a change in the activity of the serotonergic system in the brain is involved in the hypnotic action of isoflurane.

The involvement of the nociceptin receptor in the antinociceptive action of nitrous oxide.

Nociceptin and its receptor are widely expressed in the central nervous system and are involved in the modulation of nociception. We have previously reported that the minimum anesthetic alveolar concentrations for volatile anesthetics do not differ between nociceptin receptor knockout (NOP-/-) mice and wild-type (NOP+/+) mice. In the present study, we investigated whether the nociceptin system is involved in the antinociceptive action of nitrous oxide. Using the acetic acid-induced writhing test, we showed that nitrous oxide had significantly less analgesic action in NOP-/- mice than in NOP+/+ mice. Furthermore, when anesthetized with a mixture of halothane and nitrous oxide (70%), intraperitoneal injection of acetic acid resulted in an increase of plasma adrenocorticotropic hormone concentrations in NOP-/- mice but not in NOP+/+ mice. An immunohistochemical study showed that nitrous oxide exposure induced c-Fos expression in the spinal cords of NOP+/+ mice but not in those of NOP-/- mice. These results together suggest that the antinociceptive action of nitrous oxide is, at least partly, mediated by the nociceptin system.