[Usefulness of epidural anesthesia for percutaneous endoscopic lumbar discectomy (PELD)].

BACKGROUND AND METHODS: To study feasibility of epidural anesthesia for percutaneous endoscopic lumbar discectomy (PELD), we made a retrospective comparison of three anesthetic groups (28 cases with epidural anesthesia, 19 cases with local anesthesia, and 28 cases with general anesthesia) undergoing PELD. RESULTS: Three groups matched each other in age, the surgical site, and the duration of surgery; however, the frequency of male patients was significantly greater in the local anesthesia (LA) group. In the epidural anesthesia (EA) group, there was no patient who required a change of the anesthetic technique or analgesics administration during surgery. In EA group, patients received smaller amount of local anesthetic but spent longer time in the operating room compared with those in LA group. EA and GA groups included several cases staying long time in the hospital and presented wide statistical dispersion of the duration of hospitalization. There was no difference in the dose of local anesthetics, the duration of total procedure, or time to discharge between EA and GA groups. CONCLUSIONS: Epidural anesthesia is suggested to be a useful option for anesthetic techniques in patients undergoing PELD.

[Facial edema and pruritus after intravenous injection of midazolam].

Midazolam is a short-acting benzodiazepine commonly used for conscious sedation for a variety of procedures. Severe adverse reactions, including respiratory depression, respiratory arrest, and anaphylactoid reaction, have been described by manufacturers. We report a patient who developed facial edema after iv injection of midazolam during caesarian section. A 26-year-old woman with a history of atopy and pollen allergy was scheduled for caesarian section. Spinal anesthesia was induced with bupivacaine without significant medical problems. Shortly after receiving 2 mg of iv midazolam 15 minutes after delivery for conscious sedation, she developed pruritus and severe facial edema. Airway obstruction did not occur and no specific medical treatment was necessary. However she was not able to open her eyes for 8 hours because of severe eyelid swelling. We should be more careful in administering midazolam which is generally regarded as safe and well tolerated.

[Anesthesia management may alter long-term outcome-review of recent reports].

Perioperative management including anesthesia may alter long-term outcome of surgical patients. We have reviewed abstracts for meeting and articles published recently concerning effects of anesthetic depth, volatile anesthetic preconditioning, beta-blockers, alpha-agonists, statins, and glucose control on long-term outcome. Although research in this area has just been started, we, anesthesiologists should recognize its importance.

[Prostanoids and acute lung injury].

Prostanoids with various physiological effects in the lung, have been shown to be one of the important factors in acute lung injury. However, in large scale clinical studies, beneficial effects of NSAIDs or PGE1 have not been demonstrated. On the other hand, with progress of basic research in prostaglandin metabolic pathway, receptor and synthase of each prostanoid have been clarified, and selective COX-2 blockers have been developed and are now available in Japan. We reviewed the relationship between prostanoids, acute lung injury and the effects of COX-2 selective blockers, and discussed the present status and future perspective in this field.

[Effects of fentanyl on acetylcholine release from hippocampus and righting reflex in rat: an in vivo brain microdialysis study].

Fentanyl, a synthetic mu-opioid agonist, is one of the most popular opioids in clinical anesthesia. It is well-known that memory is affected by opioids and opioid antagonists in animals. Cholinergic neurones releasing acetylcholine (ACh) particularly in the hippocampus have been shown to be related to memory. This study, therefore, was conducted to examine the effects of fentanyl on hippocampal ACh release in rats. The experiments were performed on male SD rats under freely moving condition by in vivo brain microdialysis technique. After taking initial three samples, test drugs were administered. The ACh release was determined by HPLC-ECD method. Effect on behavior was determined as loss of righting reflex (LRR). Fentanyl 50, 100 and 200 micrograms.kg-1 i.p. significantly decreased the ACh release from the rat hippocampus. Naloxone, a mu-antagonist, 100 micrograms.kg-1 i.p. antagonized the inhibitory effect of fentanyl 100 micrograms.kg-1 i.p. on the ACh release in the hippocampus. Only fentanyl 200 micrograms.kg-1 i.p. produced LRR. The effects of fentanyl, the dose of which is so little that it does not produce LRR, on the rat hippocampal ACh release may be controlled by the inhibitory actions of mu-opioid receptors.

[The effects of inhaled carbon monoxide on lung injury in rats caused by lipopolysaccharide].

BACKGROUND: Carbon monoxide (CO) has long been considered a toxic substance. Recent studies have revealed that CO may play an important role in intercellular signaling. We hypothesized that CO modulates the inflammatory mechanisms. METHODS: SD rats (each study group consisting of 7 animals) inhaled 250 ppm of CO one hour prior to LPS challenges. These animals were incubated for a particular period of time (four different length of time; 1, 2, 4, and 8 hours). The control group (each study group consisting of 6 animals) had been left in the room air. Both groups were instilled with LPS (1 mg) into the lungs. At the end of each period, animals were exsanguinated, broncho-alveolar lavage (BAL) and blood sampling were performed, and a part of the small intestine was harvested. PMN numbers, protein, TNF, and IL-10 concentrations in BAL fluid were measured. Plasma TNF and IL-10 were also measured. The Wet/Dry ratio of a small intestine was calculated. RESULTS: In the CO-inhalation group, the anti-inflammatory cytokine IL-10 concentration in the BAL fluid was higher at 8 hours after LPS challenge than the counterpart of room air group (37.6 +/- 11.4 pg.ml-1 vs. 92.8 +/- 31.5 pg.ml-1, P < 0.05). W/D ratio decreased (3.29 +/- 0.2 vs. 2.94 +/- 0.06, P < 0.05). CONCLUSION: These findings indicated that CO inhalation might modulate the inflammatory response to LPS. Further study is needed to prove the therapeutic role of CO inhalation without serious adverse effects.

Effects of erythropoietin on intracellular calcium concentration of rat primary cortical neurons.

Erythropoietin (Epo) has been shown to afford neuroprotection in many experimental models. Although the cytosolic Ca(2+) concentration ([Ca(2+)](i)) is an important factor regulating cell survival, the effects of Epo on [Ca(2+)](i) in neurons are not fully elucidated. We studied the effects of human recombinant Epo on [Ca(2+)](i) of rat primary cortical neurons in normal and excitotoxic conditions. Changes in [Ca(2+)](i) were measured using fura-2 microfluorometry in rat primary cortical cultures. In the control condition with 2mM Mg(2+) in the bath solution, Epo at 4 u/ml significantly increased the fluorescence ratio, but the Epo-induced increase in the fluorescence ratio was abolished by omission of Ca(2+) from the bath solution and by the addition of cadmium. Omission of Mg(2+) and supplementation with glycine resulted in basal and periodic increases in the fluorescence ratio, due to sustained activation of N-methyl-d-asparate (NMDA) receptors. Epo at 0.4 and 4 u/ml significantly decreased the fluorescence ratio in this condition, and this effect was attenuated by the phosphoinositide 3-kinase (PI3K) inhibitors, LY 294002 and wortmannin, and the Ca-activated K channel blocker, iberiotoxin. In the presence of Mg(2+) and exogenous glutamate, 4 but not 0.4 u/ml Epo slightly but significantly reduced the [Ca(2+)](i) elevation. These results suggest that Epo increased [Ca(2+)](i) in cortical neurons by inducing Ca(2+) entry in the control condition but decreased [Ca(2+)](i) in the Mg(2+)-free excitotoxic condition, at least in part via PI3K-dependent activation of Ca-activated K channels. Reduction of [Ca(2+)](i) by Epo in the excitotoxic condition may contribute to neuroprotection.