Akiyoshi Hosoyamada

An investigation of monoamine receptors involved in antinociceptive effects of antidepressants.

We attempted to determine which monoamine re-ceptor subtypes are predominantly involved in antidepressant-induced antinociception. Antinociceptive effects were evaluated by using formalin tests with rats. Antidepressants acting as potent inhibitors of norepinephrine reuptake (nisoxetine, nortriptyline, and maprotiline) or inhibiting reuptake of both norepinephrine and serotonin (5-HT) (imipramine and milnacipran) induced dose-dependent antinociception. Simultaneous intraperitoneal administration of antidepressants and either prazosin (&agr;1 antagonist) or ketanserin (5-HT2 antagonist) significantly antagonized antinociceptive effects. Fluvoxamine (selective serotonin reuptake inhibitor) induced antinociception less potently than other antidepressants and was significantly antagonized by ketanserin, but not prazosin. Ondansetron (5-HT3 antagonist) significantly antagonized antinociception by 10 mg/kg of imipramine. In contrast, SDZ-205,557 (5-HT4 antagonist) markedly enhanced antinociception by small-dose (2.5 mg/kg) imipramine. Imipramine-induced antinociception was significantly antagonized by intracerebroventricular administration of prazosin or ketanserin, but not by yohimbine (&agr;2 antagonist) or ondansetron, and was significantly enhanced by intracerebroventricularly administered SDZ-205,557. These findings suggest that &agr;1 adrenoceptors and 5-HT2 receptors in the brain are involved in antidepressant-induced antinociception. In addition, the results suggested functional interactions between noradrenergic and serotonergic neurons as mechanisms for antidepressant-induced antinociception.

Antinociceptive efficacy of antidepressants: assessment of five antidepressants and four monoamine receptors in rats

AbstractPurpose. For assessment of the antinociceptive potency of antidepressants, we compared the antinociceptive effects of serotonin selective reuptake inhibitors (SSRIs) and classical tricyclic antidepressants (TCAs) in rats. We also attempted to elucidate the monoamine receptor subtypes predominantly involved in the antinociceptive effect of antidepressants. Methods. Male Wistar rats received SSRIs (sertraline, fluvoxamine, and citalopram) or TCAs (imipramine and desipramine) intraperitoneally, and the reaction time until pain response in the hot plate test and licking time in the formalin test were measured 60 min later. We also observed the effects of prazosin (an α1 antagonist), WB-4101 (a selective α1A antagonist), yohimbine (an α2 antagonist), WAY-100635 (a selective 5-HT1A antagonist), and ketanserin (a 5-HT2 antagonist), which were simultaneously administered with imipramine or desipramine, on the antidepressant-induced antinociceptive effect in the formalin test. Results. In the hot plate test, desipramine, 20 mg·kg−1, but not imipramine or sertraline, produced a significant increase in reaction time. In the formalin test, desipramine and imipramine produced significant reductions in the licking time at over 5 mg·kg−1 and at over 10 mg·kg−1, respectively. These reductions were nearly complete at 20 mg·kg−1. On the other hand, both SSRIs induced significant reductions in the licking time only at 20 mg·kg−1. Prazosin, WB-4101, and ketanserin significantly antagonized the antinociceptive effect of 10 mg·kg−1 of imipramine. However, imipramine-induced antinociception was not affected by yohimbine and WAY-100635. Prazosin and ketanserin also significantly suppressed antinociception by 5 mg·kg−1 of desipramine. Conclusion. These findings suggest that classical TCAs are likely to have a therapeutic advantage over SSRIs for pain control. In addition, it is likely that central α1 adrenoceptors and 5-HT2 receptors are predominantly involved in imipramine- and desipramine-induced antinociception.

Correlation of cleft type with incidence of perioperative respiratory complications in infants with cleft lip and palate.

Summary Background: A retrospective survey of 339 infants who had undergone primary plastic surgery for cleft lip and palate was performed to evaluate the concomitant preoperative assessment based on severity grading of the common cold and the correlation of cleft type with the incidence of perioperative respiratory complications.

Mandibular nerve block treatment for trismus associated with hypoxic-ischemic encephalopathy

Background and Objectives We describe the use of mandibular nerve block for the management of bilateral trismus associated with hypoxic-ischemic encephalopathy. Case Report The patient was a 65-year-old man with bilateral trismus due to hypoxic-ischemic encephalopathy. Despite his impaired consciousness, we performed fluoroscopically guided bilateral mandibular nerve block. The bilateral symptoms were sufficiently improved, without obvious side effects, by injecting a local anesthetic near the right mandibular nerve and a neurolytic near the left mandibular nerve. Conclusions Mandibular nerve block may be an effective treatment for patients with bilateral trismus due to ischemic-encephalopathy, even when consciousness is impaired.

Endoscopic thoracic sympathectomy attenuates reflex tachycardia during head-up tilt in lightly anesthetized patients with essential plamar hyperhidrosis.

AbstractPurpose. Our purpose was to examine perioperative alterations in hemodynamic changes with head-up tilt (HUT) in patients undergoing endoscopic thoracic sympathectomy (ETS). Methods. The subjects were 11 patients with essential hyperhidrosis scheduled to undergo ETS (ETS group) and 9 age-matched volunteers undergoing minor surgery (control group). HUT was performed (40°; 5 min) before and after the surgery, under nitrous oxide anesthesia. Orthostatic hypertension and hypotension in response to HUT were defined as changes of 10% or greater in systolic blood pressure. Results. The increase in heart rate in response to HUT was significantly reduced after surgery in the ETS group (from 34 ± 18 to 14 ± 11 beats·min−1; P < 0.001), but not in the control group (from 23 ± 18 to 22 ± 12 beats·min−1; P = 0.911). Orthostatic hypertension disappeared completely after ETS (from 5 of 11 to none of 11 patients; P = 0.035), whereas the prevalence of orthostatic hypotension increased significantly after ETS (from 3 of 11 to 9 of 11 patients; P = 0.030). In the control group, the prevalence of neither orthostatic hypertension nor orthostatic hypotension changed after surgery. Conclusions. ETS attenuates autonomic circulatory response under nitrous oxide anesthesia.