Published papers

Introduction: Neutrophil activation is an important process in PMN-mediated injury including ischemia-reperfusion (I/R). We hypothesized that ONO-5046, a specific neutrophil elastase inhibitor, attenuated neutrophil activation and subsequently ameliorated organ damage during VR. In the present study, we examined the effects of ONO-5046 on neutrophil activation, liver and lung injury in a rabbit model of hepatoenteric ischemia-reperfusion. Methods: With ACUC approval, eighteen rabbits underwent 30 minutes of hepatoenteric ischemia induced by cross-clamping descending aorta and 3hr of reperfusion. These animals received ertherONO-5046 (10mg/kg bolus followed by 10mg/kg/hr infusion) or vehicle (control). Neutrophil activity was assessed by luminol-dependent chemiluminescence (CL) berore crossclamp and 3hr after reperfusion. Blood lactate, plasmaAST, LDHand protein concentration of BALF were also measured. The data obtained 3hrs after reperfusion were statistically analyzed by Mann-Whitneyt and unpaired t-test. Results: No significant differences of baseline data were observed between the groups. (#p<0.05 vs Control) Control (n=9) ONO-5046 (n=9) neutrophil CL(%change vs before) 338±128% 182±70%# blood lactate(μM) 5.8±2.4 3.5±0.8# plasma AST(U/I) 417±263 149±91# plasma LDH(U/I) 1084±656 446±133# BALF protein(mg/dl) 39.9±37.4 7.3±1.7# Conclusion: Hepatoenteric ischemia-reperfusion promoted significant activation of circulating neutrophils. ONO-5046 attenuated neutrophil activation and remote organ damage during ischemia-reperfusion.

Recent reports have discussed the potential risk of transient radicular irritation (TRI) after spinal anesthesia with lidocaine. Because we have not encountered such neurologic sequelae with the high incidence reported, we prospectively examined the incidence of TRI after spinal anesthesia with lidocaine. One thousand forty-five adult patients (aged 47 ± 15 yr) receiving spinal anesthesia with 3% hyperbaric lidocaine (1.0-1.5 mL) for anorectal surgery were consecutively studied. After the induction of spinal anesthesia, all patients were placed in the prone position for surgery. Patients were evaluated for neurologic symptoms in the buttocks, thighs, or lower extremities using a checklist to standardize data collection. Although there was no complaint of neurologic symptoms on Postoperative Day (POD) 1, four patients (0.4%) reported aching, hypesthesia, numbness, or dull pain of both lower extremities and buttocks by the morning of POD 3. In three patients, the symptoms resolved without any treatment by POD 5, whereas in one patient, numbness of the lower extremities lasted until POD 7. We conclude that a combination of lidocaine with surgical position or leg manipulation during surgery might be a major contributing factor in the development of transient neurologic syndrome. Implications: Recent studies have reported the potential risk of transient neurologic syndrome after lidocaine spinal anesthesia. The current study reports a low incidence of such sequelae in 1045 patients undergoing anorectal surgery during the prone position. Other factors, such as surgical position, may be important in the development of this syndrome.

We have examined if sevoflurane anaesthesia per se modified the number of circulating leucocytes in humans. Fifty-nine patients undergoing elective surgery were anaesthetized with sevoflurane in oxygen. The inhaled concentration was increased gradually to 5% and maintained for 20 min. Arterial blood samples were obtained before induction of anaesthesia and at 20 min. While the total number of leucocytes remained constant, circulating neutrophils decreased (mean 3370 (SD 1030) mm-3 to 3170 (940) mm-3; P < 0.01) and lymphocytes increased (1870 (520) mm-3 to 2040 (580) mm-3; P < 0.01). We conclude that high concentrations of sevoflurane modified the distribution of leucocytes in anaesthetized patients.