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Background This study aimed to evaluate the effects of hypercarbia on arterial oxygenation during one-lung ventilation (OLV). Methods Fifty adult patients undergoing elective video-assisted thoracoscopic lobectomy or pneumonectomy were enrolled. Group I patients (n = 25) were first maintained at normocarbia (PaCO2: 38–42 mmHg) for 30 min and then at hypercarbia (45–50 mmHg). In Group II patients (n = 25), PaCO2 was maintained in the reverse order. Arterial oxygen partial pressure (PaO2), respiratory variables, hemodynamic variables, and hemoglobin concentration were compared during normocarbia and hypercarbia. Arterial O2 content and O2 delivery were calculated. Results PaO2 values during normocarbia and hypercarbia were 66.5 ± 10.6 and 79.7 ± 17.3 mmHg, respectively (mean difference: 13.2 mmHg, 95% CI for difference of means: 17.0 to 9.3, P < 0.001). SaO2 values during normocarbia and hypercarbia were 92.5 ± 4.8% and 94.3 ± 3.1% (P = 0.009), respectively. Static compliance of the lung (33.0 ± 5.4 vs. 30.4 ± 5.3 ml/cmH2O, P < 0.001), arterial O2 content (15.4 ± 1.4 vs. 14.9 ± 1.5 ml/dl, P < 0.001) and O2 delivery (69.9 ± 18.4 vs. 65.1 ± 18.1 ml/min, P < 0.001) were significantly higher during hypercarbia than during normocarbia. Conclusions Hypercarbia increases PaO2 and O2 carrying capacity and improves pulmonary mechanics during OLV, suggesting that it may help manage oxygenation during OLV. Therefore, permissive hypercarbia may be a simple and valuable modality to manage arterial oxygenation during OLV.

Background Repeated administration of morphine leads to characteristic tolerance. We tested the effects of intrathecal oxcarbazepine (OXC) on spinal morphine tolerance in rats using the tail flick test. Methods Sprague-Dawley rats received intrathecal injections of 10 microliter saline alone, or 10 microliter of solutions containing 100 microgram OXC, 15 microgram morphine, or OXC + morphine for 7 days. Different groups of rats received OXC on days 1-7, 1-3, or 5-7. The tail-flick assay was used to measure acute and chronic nociception. The nociceptive stimulus consisted of dipping the distal 5 cm of the tail into warm water before and 30 min after drug injection. On day 8, an antinociceptive dose-response curve was plotted, and the 50% effective dose for morphine (given alone) was determined for all groups. Results Morphine or OXC both produced acute antinociception; OXC + morphine resulted in a significantly larger response than obtained with morphine alone. Morphine tolerance was produced by intrathecal injection of morphine over 7 days. Co-administration of morphine and OXC completely blocked morphine tolerance, but tolerance developed when OXC injection was stopped, and morphine potency was partially restored by co-administration of OXC in tolerant rats. Conclusions The antinociceptive effect of both acute and chronic morphine therapy is increased with intrathecal OXC, and antinociceptive morphine tolerance is attenuated in rats.

Background: Mechanical allodynia is generally resulted from nerve damage by direct injury or inflammation. Thus, this study was designed to compare the antiallodynic effect of morphine, brimonidine and rilmenidine in two models of neuropathic pain, that is, induced by nerve ligation and neuritis. Methods: Rats were prepared with tight ligation of the L5/L6 spinal nerves (SNL group) or with Freund’s complete adjuvant (FCA) administration evoked sciatic inflammatory neuritis (SIN group). Antiallodynic effects by intrathecal morphine, brimonidine and rilmenidine were measured by applying von Frey filaments to the lesioned hind paw. Thresholds for withdrawal response were assessed and converted to % MPE to obtain an effective dose 50% (ED 50) and a dose response curve. Results: Either SNL group or SIN group showed marked mechanical allodynia in the lesioned hind paw. Antiallodynic effects of morphine were different between two groups. That is ED 50 was 0.16 μg (SIN) and 8.12 μg (SNL), and dose response curve of the SIN group shifted left from that of the SNL group. The difference between SIN and SNL groups was statistically significant (P ＜ 0.05). With the brimonidine or rilmenidine administration, ED 50 s were 0.12 μg (SNL) and 0.37 μg (SIN) and 2.16 μg (SIN) and 11.46 μg (SNL), respectively. And the shift to left of dose response curve from the SNL group is more prominent with rilmenidine administration. Conclusions: These results suggest morphine and rilmenidine showed a better effect on reducing the mechanical allodynia induced by FCA administration. (Korean J Anesthesiol 2009; 56: 425～32)

A 56-year-old man with a rotator cuff injury, scheduled for arthroscopic reconstruction surgery, had a history of recurrent symptoms of eyeball pain and blurred vision for several years. After close examination, he was diagnosed with Posner-Schlossman syndrome. Three weeks before the scheduled surgery, his intraocular pressure (IOP) increased (> 30 mmHg) and he became extremely anxious about the surgery. We monitored his IOP intraoperatively and successfully completed general anesthesia without any sequelae. As Posner-Schlossman syndrome can present with severe complications that may lead to postoperative visual loss, intraoperative monitoring of intraocular monitoring and careful anesthetic management are crucial to protect vision.

Resection of large sacrococcygeal teratomas (SCTs) in premature neonates has been associated with significant perinatal mortality, making this a high risk procedure requiring careful anesthetic management. Most deaths during resection of SCTs are due to cardiac arrest caused by electrolyte imbalances, such as hyperkalemia, and massive bleeding during surgery. We describe two premature neonates who experienced cardiac arrest, one due to hyperkalemia and the other not due to hyperkalemia, during excision of large, prenatally diagnosed SCTs. We present here the considerations for anesthesia in premature neonates with huge SCTs.

Background: We examined the usefulness of respiratory pulse transit time (PTT) variation as an intravascular volume index in young, healthy, spontaneous, paced breathing volunteers exposed to simulated central hypovolemia by lower body negative pressure (LBNP). Methods: With paced breathing at 0.25 Hz, beat-to-beat finger blood pressure (BP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), and PTT were measured non-invasively in 18 healthy volunteers. Graded central hypovolemia was generated using LBNP from 0 to −20, −30, −40, and −50 mmHg. Respiratory PTT variation (PTTV) was calculated as the difference of maximal and minimal values divided by their respective means. Respiratory-frequency PTT variability (PTTRF) using power spectral analysis was also estimated. Results: During LBNP, SV, CO and PTTRF decreased, but PTT, PTTV and TPR increased significantly. PTTV did not correlate with SV changes (r = −0.08, P = 0.52), but PTTRF (r = 0.58, P ＜ 0.01) and PTT (r = 0.43, P ＜ 0.01) did during progressive hypovolemia. Conclusions: PTTRF is more applicable to the changes in intravascular volume than PTT and PTTV, suggesting spectral analysis of PTT might be used as a dynamic preload index in patients with spontaneous and paced breathing condition, which needs further studies. (Korean J Anesthesiol 2009; 56: 265～72)

Background Chronic administration of morphine leads to the development of tolerance. We investigated the effects of intrathecal lamotrigine on the spinal morphine tolerance in rats that are undergoing tail flick tests. Methods Sprague-Dawley rats were given intrathecal injections of saline 10 microl, lamotrigine 300 microg, morphine 15 microg or lamotrigine plus morphine combinations for 7 days (lamotrigine was given for days 1-7, days 1-3 or days 5-7). The acute and chronic nociceptive sensitivities were assessed using a tail flick test in which the distal 5 cm of the tail was dipped into warm water before and 30 minutes after the drug injection. With successive injections of morphine on day 8, a cumulative antinociceptive dose-response curve was constructed and the 50% effective dose (ED50) was calculated for each study group. Results The coinjection group of lamotrigine with morphine blocked the development of tolerance, as was shown by the preservation of morphine antinociception over 7 days and the concomitant decrease in the ED50 values on day 8, as compared with the morphine-alone group. Coinjection of lamotrigine blocked the development of morphine tolerance, as shown by the preservation of morphine antinociception over 7 days and the concomitant decrease in the ED50 values on day 8, as compared with the morphine-alone group. Conclusions This study suggests that lamotrigine augments the antinociceptive action of both acute and chronic morphine therapy, and it also attenuates the antinociceptive morphine tolerance in rats.

Nerve injury may produce a tactile allodynia. However, there are few reports regarding the interaction of morphine and selective serotonin reuptake inhibitors (SSRIs) during a neuropathic pain state. Therefore, we investigated the antiallodynic interaction between morphine and SSRIs in a rat model of neuropathic pain. Methods: Rats were prepared with a tight ligation of the left fifth and sixth lumbar spinal nerves and chronic intrathecal catheter implantation. Mechanical allodynia was then measured by application of von Frey filaments. Morphine, citalopram and paroxetine were administered intrathecally to obtain the dose-response curves. The 50% effective dose of morphine and citalopram or paroxetine were then coadministered to evaluate the drug interaction. In addition, naloxone and methysergide were administered to examine the reversal of the antiallodynic effect. Results: Intrathecal morphine produced a dose-dependent antagonism of the tactile allodynia, but intrathecal citalopram or paroxetine showed no antiallodynic effects. In addition, a morphine-citalopram or paroxetine combination produced an increase in the withdrawal threshold, but naloxone and methysergide reversed the antiallodynic effect. In addition, no interactions were observed between naloxone and citalopram or paroxetine, or morphine and methysergide. Conclusions: These results suggest that activation of both μ-opioid and serotonin receptors is required for the increased interaction to occur between morphine and SSRIs administered to reduce tactile allodynia. Thus, serotonin receptors take part in the antiallodynic action of morphine at the spinal level.

Analgesic tolerance to opioids has been described in both experimental and clinical conditions, which may limit their clinical utility. This study investigated the effects of intrathecal adenosine A1 receptor agonist (R-PIA) on spinal morphine tolerance. Methods: SD rats were given intrathecal injections of saline 10μl, R-PIA 10μg, morphine 10μg, or R-PIA plus morphine combinations for 7 days (R-PIA given for days 1-7; days 1-3; or days 5-7). Antiallodynic testing using von Frey filaments was carried out before and 30 minutes after the drug injection. On day 8, an antiallodynic dose-response curve was constructed and the 50% effective dose (ED50) for morphine (given alone) was calculated for each study group. Results: The coinjection group of R-PIA with morphine blocked the development of tolerance, as shown by the preservation of morphine antiallodynia over 7 days the concomitant decrease in the ED50 values on day 8, compared with the morphine-alone group. Although additive analgesia over days 1-7 cannot be ruled out, the reductions of the ED50 in the R-PIA and morphine combination group suggest some suppression of tolerance. Conclusions: These results suggest that intrathecal R-PIA prevents the development of spinal opioid tolerance. Future studies will be needed to examine the respective roles of supraspinal and peripheral sites of R-PIA and morphine interaction, and to investigate the mechanisms underlying the action of R-PIA on opioid tolerance.

S 36 Received:April 27, 2007 Corresponding to:Jai Hyun Hwang, Department of Anesthesiology and Pain Medicine, Asan Medical Center, 388-1, Pungnap 2-dong, Songpa-gu, Seoul 138-736, Korea. Tel: 82-2-3010-3859, Fax: 82-2-470-1363, E-mail: jhhwang@amc.seoul.kr This study was supported by a grant (# 03-153) from Asan Institute for Life Sciences, Seoul, Korea. Effect of Administering Freund’s Complete Adjuvant to Spinal Nerves on the Development of Allodynia in the Rat

Background: Marked changes in systemic hemodynamics during liver transplantation may lead to changes in cerebral hemodynamics and metabolism. Therefore, continuous monitoring of the jugular venous oxygen saturation (SjvO2) may help the anesthetic management of liver transplantation. Methods: We observed changes in SjvO2 using a double lumen oximetry catheter for continuous monitoring and analyzed the correlation between SjvO2 and hemodynamic measurements in thirty patients undergoing liver transplantation. Results: There were no significant changes in SjvO2 compared to initial SjvO2 during liver transplantation. SjvO2, however, increased from 72.5 to 79.6 % (P ＜ 0.05), before and after reperfusion. There was a weak correlation between changes in SjvO2 and cardiac output (r = 0.38, P ＜ 0.05), whereas no correlation was found among changes in SjvO2 and arterial carbon dioxide tension, mean arterial pressure, central venous pressure, or mixed venous oxygen saturation before and after reperfusion. Conclusions: SjvO2 that reflects changes in cerebral oxygen demand-supply balance was well maintained during liver transplantation except the reperfusion period. Continuous monitoring of changes in SjvO2 at this period may provide further insight to understand physiology of cerebral oxygenation during liver transplantation and merits further studies. (Korean J Anesthesiol 2006; 51: 578～83)

Ex situ resection of the liver is an alternative surgical procedure for patients with conventionally unresectable hepatic tumors, and with contraindications to liver transplantation. We experienced a case of ex situ resection of the liver in a 40-year-old female patient suffering from sclerosing hepatocellular carcinoma. Preoperative liver function was normal. The duration of the anhepatic period was 2 hours and 55 minutes. No severe hemodynamic or pulmonary complications, and no significant metabolic or coagulatory disorders occurred. To obtain good results by ex situ resection of the liver, anesthesiologist should understand the physiology of the anhepatic period and guard against possible problems during the operation.

Background: Laryngoscopy, tracheal intubation and the suspension laryngoscopy often provoke an undesirable increase in blood pressure and/or heart rate during laryngeal microscopic surgery. Thus, the anesthesiologist's objectives are to maintain sufficient anesthetic depth and to promote rapid awakening. Nicardipine, a direct arterial dilator, can be used to attenuate increasing blood pressure. We investigated the effects of nicardipine on changes of blood pressure and heart rate during laryngeal microscopic surgery. Methods: Eighty patients of ASA class 1 or 2 scheduled for laryngeal microscopic surgery were randomly allocated into 4 groups. For anesthetic induction, IV propofol 1.5 mg/kg, rocuronium 0.4 mg/kg, and glycopyrrolate 0.2 mg were administered followed by mask ventilation for 5 minutes with isoflurane. One minute before tracheal intubation and suspension laryngoscopy saline, nicardipine 10, 20, or 30/kg was injected in each group. Thereafter we measured blood pressure and heart rate one minute after each procedure. Results: Increases in blood pressure were blunted in the nicardipine 20 and 30/kg group. In the nicardipine 30/kg group, heart rates were significantly increased and facial flushing was observed in two patients. Conclusions: We suggest that nicardipine 20/kg can alleviate blood pressure increases with little effect on heart rate during laryngeal microscopic surgery. However, although nicardipine 30/kg could blunt blood pressure increases, it produces tachycardia and perhaps overdose.

Case 1: A 30-year-old woman was scheduled for mitral valvuloplasty. A pulmonary artery (PA) catheter (Swan-Ganz CCOmbo model: 744HF75, Edwards, USA) was inserted via an introducer (8.5 Fr) placed in the right external jugular vein. The tip of the catheter could not be passed from the external jugular vein to the subclavian vein. When we attempted to advance the PA catheter again 30 minutes later, it could not be advanced or withdrawn. The PA catheter was removed with an introducer. The tip of the introducer had curled up into the intralummial space and the PA catheter had impacted in the narrowed lumen. Case 2: A 48-year-old woman was scheduled for tricuspid annuloplasty. A PA catheter was inserted via an introducer placed in the right internal jugular vein without problem. After opening the right atrium and withdrawing the PA catheter, a vinyl strip was found to have torn away from the distal part of the PA catheter.

Background: A Nerve ligation injury may produce a pain syndrome that includes tactile allodynia. Reversal effects on tactile allodynia have been demonstrated after an intrathecal administration of adenosine analogues or morphine. Adenosine receptor agonists have been known to have antinociceptive and antiallodynic effects in many animal and human studies. We examined the drug interactions between morphine and adenosine agonists in a rat model of a nerve ligation injury. Methods: Male Sprague Dawley rats were prepared with a tight ligation of the left lumbar 5 th and 6 th spinal nerves and chronic lumbar intrathecal catheter implantation for drug administration. We measured the tactile allodynia by applying von Frey filaments ipsilateral to the lesioned hindpaw. Thresholds for paw withdrawal were assessed. Morphine (1-30g), adenosine (1-30g) and R-PIA (0.1-10g) were administered to obtain the dose-response curves and the 50% effective dose (ED50). Fractions of ED50 values were administered to establish the ED50 of drug combinations. Drug interactions were evaluated by the fractional and isobolographic analyses. Allodynic thresholds for left lesioned hindpaw withdrawal to the von Frey hairs test were assessed and converted to % maximal possible effect (%MPE). Results: The antiallodynic effect of morphine, adenosine, and R-PIA were produced in a dose dependent manner. The antiallodynic effects of combinations showed a similar pattern. Isobolographic analysis revealed a synergistic interaction for the morphine-R-PIA combination but not for the morphine-adenosine combination. However, fractional analysis produced a synergistic result for two combination groups. Conclusions: The results demonstrated that intrathecal co-administration of adenosine A1 receptors agonist and morphine showed the synergistic effect on nerve ligation injury induced allodynia.

Background: A spinal nerve ligation (SNL) injury may produce a neuropathic pain syndrome that includes tactile allodynia. This pain state may be diminished by sympathectomy. Intradermal (I.D.) injection of norepinephrine (NE) evokes pain in patients with sympathetically maintained pain. Recently, we reported the effect of intrathecal (I.T.) brimonidine and rilmenidine on the sympathetic nervous system. Therefore, we conducted a behavioral test to investigate the effects of sympathetic stimulation by I.D. NE on mechanical allodynia in rats with a SNL injury. Methods: Male SD rats were prepared with ligation of the left lumbar 5th and 6th spinal nerves and lumbar I.T. catheter implantation. NE 10g I.D. was administered in normal and SNL rats to investigate the change of cutaneous sensitivity to tactile stimuli. NE 30g I.D. was administered before and after I.T. injection of brimonidine 3g and rilmenidine 30g in SNL rats. Using a von Frey hair (VFH) test, we examined the effects of NE on the withdrawal threshold. Allodynic thresholds for the withdrawal response of the lesioned hindpaw to VFH stimuli were assessed. Results: Intradermal NE produced a reduction of the withdrawal threshold in normal and allodynic rats. An allodynic state induced by a SNL was aggravated by NE. In allodynic rats, the baseline threshold of a lesioned left hindpaw was markedly low and such a state was maintained during the behavioral experiment. The antiallodynic effects of I.T. brimonidine and rilmenidine were produced in both pre- and post-treatment of NE. Conclusions: The results suggest that a sympathetic component is likely involved in the mechanism of mechanical allodynia produced by a SNL injury.

Background: Although the efficacy of morphine in a neuropathic pain state is somewhat controversial, intrathecally administered morphine reversed the mechanical allodynia in a previous animal study. Using a behavioral test, we investigated the mechanism of the antiallodynic action of intrathecal morphine by administering opioids, α2 adrenergic and cholinergic receptor antagonists in a rat model of neuropathic pain induced by a spinal nerve ligation injury. Methods: Male Sprague Dawley rats were prepared with a tigh1 ligation of the left lumbar 5th and 6th spinal nerves and insertion of a chronic lumbar intrathecal catheter. Morphine 1 μg was administered intrathecally to attenuate the mechanical allodynic. Naloxane 10 μg, yohimbine 30 μg, prazosin 30 μg, atropine 10 μg, pirenzepine 10 μg, and methoctramine 10 μg was administered intrathecally before and after the injection of morphine in order to investigate the reversal of an increased allodynic threshold by morphine. The allodynic thresholds for the left hindpaw withdrawal to von Frey hairs were assessed and converted to %MPE. Results: A reduction of mechanical alladynia by intrathecal morphine was produced. Naloxone pretreatment, but not posttreatment, reversed the antiallodynic effect of intrathecal morphine (P < 0.01). All α2 adrenergic and cholinergic receptor antagonists used here did not reverse it. Conclusions: The results suggest that the reversal mechanism of mechanical allodynia by intrathecal morphine appears to be mediated mostly by the opioid receptor system, but not the α2 adrcenergic and cholinergic receptor systems, at the spinal level in a rat model of e spinal nerve ligation injury.

Background: Clonidine, an α2 adrenoceptor agonist, has been known to have antinociceptive and antiallodynic effects. The antinociceptive and antiallodynic effects of brimonidine, a new selective α2 agonist, have not been evaluated yet in rats. Behavioral tests were performed to investigate the effects of systemically and spinally administered brimonidine on nociception and mechanical allodynia and the effect of spinal nerve ligation (SNL) on antinociception. Methods: Rats were prepared with tight ligation of spinal nerves and/or a lumbar intrathecal catheter implantation. Using a hot plate (HP) test or von Frey hair (VFH) test, the effect of intraperitoneal (I.P.) and intrathecal (I.T.) brimonidine in normal and SNL rats were examined. I.P. brimonidine (100-1,000 μg) and I.T. brimonidine (0.1-3.0μg) were given to examine the antinociceptive effect on an HP test. After a SNL, a HP test was conducted at the same doses of brimonidine to compare with the preoperative state. I.T. brimonidine (0.03-3.0μg) and saline (control) were administered to examine the antiallodynic effect in SNL rats. In addition, an antagonistic study with yohimbine 1.0 mg/kg I.P. was performed to investigate the reversal of the antiallodynic effect of brimonidine. Allodynic thresholds for lesioned hindpaw withdrawl to a VFH test were assessed and converted to %MPE. Results: I.P. brimonidine produced an antinociceptive effect, and I.T. brimonidine also produced a significant antinociceptive effect (P < 0.05). After an SNL, I.T. brimonidine produced a dose-dependent antinocicpetive effect. In addition, I.T. brimonidine produced a dose-dependent antiallodynic effect which is antagonized by yohimbine (P < 0.05). Conclusions: The results suggest that brimonidine has a more potent antiallodynic effect when given intrathecally. (Korean J Anesthesiol 2001; 40: 397∼405) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ

Background: Pulmonary hypertension (PH) associated with end stage liver disease is rare but the risk of hemodynamic deterioration during liver transplantation may be high. This study was done to characterize the pulmonary hemodynamics during liver transplantation and to seek the relationship between pulmonary artery pressure (PAP) and other hemodynamic variables. Methods: One hundred patients undergoing liver transplantation were chosen and we divided patients into normal and PH groups (mean pulmonary artery pressure [MPAP] > 25 mmHg). Hemodynamic data was collected throughout the surgery. Studied variables between groups were analyzed with an unpaired t-test. The relationship between MPAP and other hemodynamic variables was analyzed with a linear regression test. Survival analysis was performed by cumulative survival analysis (Logrank test). Results: Incidence of PH during liver transplantation was 34%, and true PH (pulmonary vascular resistance index [PVRI] > 150 dyne.sec/cm/m, MPAP > 25 mmHg) was 7%. MPAP, systemic vascular resistance index, cardiac index, right ventricular ejection fraction, maximum elastance, central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP), and right ventricular end-diastolic volume index were significantly higher in the PH group. In the PH group, right ventricular function curve was abnormal. MPAP correlated significantly with PAOP, and CVP (P < 0.01). One year survival rate showed no significant difference between groups (Logrank test P = 0.49). Conclusions: Episodes of increased pulmonary artery pressure during liver transplantation was not infrequent. PAP was more dependent on preloads. In patients with high PAP, RV diastolic dysfunction was usually observed. Early mortality rate after liver transplantation was not associated with PH. (Korean J Anesthesiol 2001; 40: 340∼347) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ

Background: Clonidine, an α2 adrenoceptor agonist, has been known to have an antialladynic effect in many animal and human studies. Clonidine, however, acts on imidazoline receptors as well as α2 adrenoceptors, Recently, the effect of clonidine on the symapthetic nervous system was reported to be mediated via the activation of the imidazoline receptor system but not the α2 adrenergic receptor system. Therefore, we conducted a behavioral test to investigate the effects of α 2 adrenoceptors and imidazoline receptors on mechanical allodynia in rats with spinal nerve ligation (SNL) injury. Methods: Male Sprague Dawley rats were prepared with tight ligation of the left lumbar 5th and 6th spinal nerves and chronic lumbar intrathecal catheter implantation for drug administration. Using a von Frey hair (VFH) test, we examined the effects of intrathecal (IT) brimonidine (0,03-3 μg), clonidine (3-10 μg), and rilmenidine (1-30 μg) in SNL rats. Measurements of the baseline value VFH test was conducted at each dose to compare with the preoperative state. In addition, an antagonistic study with rauwolscine or yohimbine was performed to investigate the reversal of antiallodynic effects of each agonist. Allodynic thresholds for the withdrawal response of the left lesioned hindpaw to VFH stimuli were assessed and convetted to %MPE. Results: The antiallodynic effects of brimonidine, clonidine, and rilmenidine were produced in a dose dependent manner. The antiallodynic effects of IT brimonidine but not rilmenidine were significantly antagonized by α2 antgonists rauwolscine and yohimbine (P < 0.05), Conclusions: The results suggest that mechanical allodynia produced by a SNL injury is reduced by an imidazoline receptor agonist as well as α2 adrenergic receptor agonists and sympathetic activation is more likely mediated by spinal imidazoline receptors.