Intrathecal bupivacaine protects against extension of lesions in an acute contusive spinal cord injury model

BACKGROUND AND OBJECTIVE: We recently demonstrated that intrathecal bupivacaine before or after acute photochemical spinal injury improved functional outcome in rats. However, the closest model to spinal trauma is the contusive weight-drop method. The aim of this study was to evaluate functional, electrophysiological and anatomical consequences of a contusive spinal-cord lesion in rats with or without an intrathecal injection of bupivacaine. METHODS: Fifteen minutes before a contusive spinal lesion, 18 rats received intrathecally either 0.5% bupivacaine (Group T) or saline (Group C). During an 18-days period, motor and sensory functions were evaluated, and bladder voiding dysfunction was noted. Somatosensory evoked potential testings were performed at day 18. Then, the intact spinal cord area at the epicentre of the lesion and the extent of the lesion were measured. RESULTS: Motor deficit was less and inclined-plane stability was better in treated animals at all times, the scores were statistically different from day 7. There were no differences concerning the sensory test. Despite no significant difference, there were less spinal bladders in the T group from day 7. Somatosensory evoked potential latencies were longer in T group, but only the first negative component (N1) was statistically significant. Amplitudes were higher in T group, but were not statistically different. The spinal cord intact area at the epicentre of the lesion was higher in the T group (1.23 +/- 0.8 mm(2) vs. 0.81 +/- 0.39 mm(2); P < 0.05). The extent of the lesion was higher in the C group (9.4 +/- 2.9 mm vs. 6.4 +/- 3.4 mm; P < 0.05). CONCLUSION: Intrathecal 0.5% bupivacaine provide a neuroprotective effect by decreasing functional, electrophysiological and anatomical consequences after a contusive spinal cord injury.     

The analgesic and sedative effects of intrathecal midazolam in perianal surgery

BACKGROUND AND OBJECTIVE: Our purpose was to evaluate the analgesic and sedative effects of intrathecal midazolam when added to spinal bupivacaine in patients undergoing perianal surgery under spinal anaesthesia. METHODS: Forty-four patients were randomly allocated into two equal groups: Group I (B) received hyperbaric bupivacaine 0.5% 2 mL + saline 0.9% 1 mL in a total volume of 3 mL intrathecally; Group II (BM) received hyperbaric bupivacaine 0.5% 2 mL + 1 mL of 2mg preservative-free midazolam in a total volume of 3 mL intrathecally. In both groups, the onset and recovery times of sensory block, the degree and recovery times of motor block as well as the sedation and visual analogue pain scores were recorded, and statistically compared. RESULTS: In Group BM, the postoperative visual analogue pain scores were significantly lower at the first 4 h (P < 0.05), the average time until the first dose of additional analgesic requirement was significantly longer (P < 0.05), and sedation scales were significantly higher (P < 0.05), compared to Group B. There were no statistically significant differences in the onset and the full recovery times of sensory and motor blocks in the two groups. CONCLUSION: The use of intrathecal midazolam combined with intrathecal bupivacaine produces a more effective and longer analgesia with a mild sedative effect in perianal surgery.     

Neuraxial morphine may trigger transient motor dysfunction after a noninjurious interval of spinal cord ischemia: a clinical and experimental study

BACKGROUND: A patient underwent repair of a thoracoabdominal aortic aneurysm. Epidural morphine, 4 mg, was given for pain relief. After anesthesia, the patient displayed lower extremity paraparesis. This effect was reversed by naloxone. The authors sought to confirm these observations using a rat spinal ischemia model to define the effects of intrathecal morphine administered at various times after reflow on behavior and spinal histopathology. METHODS: Spinal cord ischemia was induced for 6 min using an intraaortic balloon. Morphine or saline, 30 microg, was injected intrathecally at 0.5, 2, or 24 h after reflow. In a separate group, spinal cord temperature was decreased to 27 degrees C before ischemia. After ischemia, recovery of motor function was assessed periodically using the motor deficit index (0 = complete recovery; 6 = complete paraplegia). RESULTS: After ischemia, all rats showed near-complete recovery of function by 4-6 h. Intrathecal injection of morphine at 0.5 or 2 h of reflow (but not at 24 h) but not saline caused a development of hind limb dysfunction and lasted for 4.5 h (motor deficit index score = 4-6). This effect was reversed by intrathecal naloxone (30 microg). Intrathecal morphine administered after hypothermic ischemia was without effect. Histopathological analysis in animals that received intrathecal morphine at 0.5 or 2 h after ischemia (but not at 24 h) revealed dark-staining alpha motoneurons and interneurons. Intrathecal saline or spinal hypothermia plus morphine was without effect. CONCLUSIONS: These data indicate that during the immediate reflow following a noninjurious interval of spinal ischemia, intrathecal morphine potentiates motor dysfunction. Reversal by naloxone suggests that this effect results from an opioid receptor-mediated potentiation of a transient block of inhibitory neurons initiated by spinal ischemia.     

The time course of acquisition of ischemic tolerance and induction of heat shock protein 70 after a brief period of ischemia in the spinal cord in rabbits

We examined the time course of development of ischemic tolerance in the spinal cord and sought its mechanism exploring the expression of heat shock protein 70 (HSP70). Spinal cord ischemia was produced in rabbits by occlusion of the abdominal aorta. In Experiment 1, neurologic and histopathologic outcome was evaluated 48 h after prolonged ischemia (20 min) that was given 2 days, 4 days, or 7 days after a short period of ischemia (ischemic pretreatment) sufficient to abolish postsynaptic component of spinal cord evoked potentials. Control animals were given prolonged ischemia 4 days after sham operation. In Experiment 2, HSP70 expression in motor neurons after pretreatment without exposure to prolonged ischemia was examined by immunohistochemical staining. Ischemic pretreatment 4 days (but not 2 days or 7 days) before 20 min ischemia exhibited protective effects against spinal cord injury. In the cytoplasm, HSP70 immunoreactivity was mildly increased after 2, 4, and 7 days of ischemic pretreatment. However, the incidence of nuclear HSP70 immunoreactivity 2 days, 4 days, and 7 days after ischemic pretreatment was 2 of 6 animals, 4 of 6 animals, and 1 of 6 animals, respectively (none in the control group). These results suggest that ischemic tolerance is apparent 4 days after ischemic pretreatment and that HSP70 immunoreactivity in the nucleus may provide some insight into the mechanisms of ischemic tolerance in the spinal cord.     

Neuraxial Morphine May Trigger Transient Motor Dysfunction after a Noninjurious Interval of Spinal Cord Ischemia: A Clinical and Experimental Study

Background: A patient underwent repair of a thoracoabdominal aortic aneurysm. Epidural morphine, 4 mg, was given for pain relief. After anesthesia, the patient displayed lower extremity paraparesis. This effect was reversed by naloxone. The authors sought to confirm these observations using a rat spinal ischemia model to define the effects of intrathecal morphine administered at various times after reflow on behavior and spinal histopathology.

Methods: Spinal cord ischemia was induced for 6 min using an intraaortic balloon. Morphine or saline, 30 [mu]g, was injected intrathecally at 0.5, 2, or 24 h after reflow. In a separate group, spinal cord temperature was decreased to 27[degrees]C before ischemia. After ischemia, recovery of motor function was assessed periodically using the motor deficit index (0 = complete recovery; 6 = complete paraplegia).

Results: After ischemia, all rats showed near-complete recovery of function by 4-6 h. Intrathecal injection of morphine at 0.5 or 2 h of reflow (but not at 24 h) but not saline caused a development of hind limb dysfunction and lasted for 4.5 h (motor deficit index score = 4-6). This effect was reversed by intrathecal naloxone (30 [mu]g). Intrathecal morphine administered after hypothermic ischemia was without effect. Histopathological analysis in animals that received intrathecal morphine at 0.5 or 2 h after ischemia (but not at 24 h) revealed dark-staining [alpha] motoneurons and interneurons. Intrathecal saline or spinal hypothermia plus morphine was without effect.     

Intrathecal midazolam added to bupivacaine improves the duration and quality of spinal anaesthesia

BACKGROUND: The antinociceptive action of intrathecal midazolam is well documented. In this prospective study, we investigated the addition of midazolam to intrathecal bupivacaine on the duration and quality of spinal blockade. METHODS: Forty ASA I or II adult patients undergoing lower abdominal surgery were selected for the study. The patients were randomly allocated to receive 3 ml of 0.5% hyperbaric bupivacaine intrathecally either alone or with 1 mg of midazolam using a combined spinal epidural technique. The duration and quality of sensory and motor block, perioperative analgesia, haemodynamic changes, and sedation levels were assessed. RESULTS: The duration of sensory block (i.e. time to regression to the S2 segment) was significantly longer in the midazolam group than the control group (218 min vs. 165 min; P < 0.001). The duration of motor block was also prolonged in the midazolam group as compared with the control group (P < 0.01). In 90% of the patients in the midazolam group, the quality of block was adequate during the intra-operative period as compared with only 65% of the patients in the control group (P < 0.05). The duration of effective analgesia was longer in the midazolam group than in the control group (199 vs. 103 min; P < 0.001). Blood pressure, heart rate, oxygen saturation and sedation scores were comparable in both groups. No neurological deficit or other significant adverse effects were recorded. CONCLUSION: The addition of intrathecal midazolam to bupivacaine significantly improves the duration and quality of spinal anaesthesia and provides prolonged perioperative analgesia without significant side-effects.     

Mild hypothermia reduces expression of heat shock protein 60 in leukocytes from severely head-injured patients

BACKGROUND: Infectious complications are among the most serious problems that occur in severely head-injured patients treated with mild hypothermia. The mechanism underlying the susceptibility to infection has not been clarified. Heat shock protein (HSP) 60 has been reported to play an essential role in innate immunity. Thus, we conducted a study to clarify the impact of mild hypothermia on the expression of HSPs in polymorphonuclear leukocytes (PMNLs) in severely head-injured patients. METHODS: Between September 1997 and November 1999, 17 severely head-injured patients with a Glasgow Coma Scale score of 8 or less at admission in whom intracranial pressure could be maintained below 20 mm Hg by conventional therapy were randomly assigned to two treatment groups: a mild hypothermia group (HT group, nine patients) and a normothermia group (NT group, eight patients). The HT group was subjected to mild hypothermia (intracranial temperature, 34 degrees C) for 48 hours followed by rewarming at a rate of 1 degrees C per day for 3 days, whereas the NT group was subjected to normothermia (intracranial temperature, 37 degrees C) for 5 days. Blood samples were serially obtained at three time points; days 0 to 1, days 2 to 5, and days 6 to 14 after head injury. We measured the expression of HSP27, HSP60, HSP70, and HSP90 by flow cytometry. RESULTS: The two groups were similar with respect to prognostic factors, and there was no difference in clinical outcome. The expression of PMNL HSP60 in the HT group was significantly lower in all three time periods compared with that in the NT group (p < 0.05), whereas expression of the other HSPs did not differ significantly between the groups. The incidence of infectious complications was significantly increased in the HT group over that in the NT group (p < 0.05). In in vitro studies, PMNLs from 10 healthy volunteers were incubated at 37 degrees C, 34 degrees C, or 26 degrees C for 1 hour with sodium arsenite (100 micromol/L), an HSP inducer. The expression of HSP60 at 26 degrees C and 34 degrees C was significantly lower than that at 37 degrees C (p < 0.05), whereas expression of the other HSPs did not differ significantly at 26 degrees C, 34 degrees C, or 37 degrees C. CONCLUSION: Mild hypothermia reduces the expression of HSP60 in PMNLs from severely head-injured patients. Thus, mild hypothermia may suppress innate immunity.     

Combined spinal-epidural anesthesia using epidural volume extension leads to faster motor recovery after elective cesarean delivery: a prospective, randomized, double-blind study

Epidural volume extension (EVE) via a combined spinal-epidural (CSE) technique is the enhancement of a small-dose intrathecal block by epidural saline boluses. In this prospective, randomized, double-blind study, we compared the EVE technique with single-shot spinal anesthesia with respect to its sensory and motor block profile and hemodynamic stability. Sixty-two parturients (n = 31 in each group) undergoing elective cesarean deliveries were administered either spinal anesthesia with hyperbaric 0.5% bupivacaine 9 mg and fentanyl 10 microg or CSE comprising intrathecal hyperbaric 0.5% bupivacaine 5 mg with fentanyl 10 microg, followed by 0.9% saline 6.0 mL through the epidural catheter 5 min thereafter. In each group, the lowest systolic blood pressure (SBP), sensory block level to loss of pain from pinprick, and modified Bromage scores were recorded at 2.5-min intervals. The visual analog pain score (VAS), peak sensory block height, highest modified Bromage motor score, time for sensory regression to the tenth thoracic dermatome (T10), and motor block recovery were compared between groups. Both groups were comparable in demographic data, VAS scores, peak sensory block height, time for sensory regression to T10, and lowest SBP recorded. Patients in the EVE group demonstrated significantly faster motor recovery to modified Bromage 0 (73 +/- 33 min versus 136 +/- 32 min, P < 0.05). IMPLICATIONS: When compared with conventional, single-shot spinal anesthesia, epidural volume extension of a small-dose spinal block provides satisfactory anesthesia for cesarean delivery with only 55% of the bupivacaine dose required and is associated with faster motor recovery of the lower limbs.     

An evaluation of intrathecal bupivacaine combined with intrathecal or intravenous clonidine in children undergoing orthopedic surgery: a randomized double-blinded study

Background: Propofol is a popular agent for providing intraoperative sedation in pediatric population during lumbar puncture and spinal anesthesia. Adjuvant‐like clonidine is used increasingly in pediatric anesthesia to provide postoperative analgesia with a local anesthetic agent. The aim of this study was to assess the effects of intrathecal and intravenous clonidine on postoperative analgesia/sedation and intraoperative requirements of propofol after intrathecal bupivacaine for orthopedic surgery in children. Methods: Fifty‐nine ASA I and II children aged 6–8 year undergoing orthopedic surgery were randomized to receive intrathecal 0.5% bupivacaine 0.2–0.4 mg·kg^?1 and intravenous 2 ml saline (Group B), intrathecal 0.5% bupivacaine 0.2–0.4 mg·kg^?1 plus 1 μg·kg^?1 clonidine and intravenous 2 ml saline (Group BCit), and 0.5% bupivacaine 0.2–0.4 mg·kg^?1 and intravenous 1 μg·kg^?1 clonidine in 2 ml of saline (Group BCiv). Intraoperative sedation was maintained with 20–50 μg·kg^?1·min^?1 of propofol infusion. The requirements of propofol, time to first rescue analgesia, and postoperative pain or sedation scores were assessed. The duration of motor and sensory blocks and perioperative adverse events were determined. Results: Clonidine significantly prolonged the time to first rescue analgesia and reduced the requirements of propofol sedation whether administered intravenously or intrathecally. The mean Children and Infants Postoperative Pain Scale scores of children were significantly lower in groups BCit and BCiv than in group B. Postoperative sedation scores were higher in groups BCit and BCiv than in group B. Intrathecal clonidine significantly prolonged the time to regression of the sensory block and recovery of motor block. There were no significant differences among the three groups regarding the incidence of perioperative adverse events. Conclusion: Intrathecal or intravenous clonidine similarly provided better postoperative analgesia and sedation and reduced the requirements of propofol. Only intrathecal clonidine prolonged the duration of sensory and motor blocks.     

全髋关节置换术老年患者轻比重布比卡因单侧连续腰麻的效果

目的 评价全髋关节置换术老年患者轻比重布比卡因单侧连续腰麻的效果.方法 拟行全髋关节置换术的老年患者60例,年龄69～98岁,性别不限,ASA Ⅱ或Ⅲ级,体重46～81 kg,随机分为2组(n=30):轻比重布比卡因组(HB组)和等比重布比卡因组(IB组).HB组和IB组分别以0.1 ml/s的速率蛛网膜下腔注入0.5%轻比重布比卡因或0.5%等比重布比卡因各1 ml.每隔5 min测定麻醉平面和感觉、运动阻滞程度,每次追加0.5%布比卡因0.5 ml,维持麻醉平面T_8～T_(10).于注药前和麻醉平面达T_8～T_(10)时,记录血压、平均动脉压和心率;记录术中不良反应的发生情况、布比卡因用量、患肢的有效镇痛时间、有效运动阻滞时间和术后并发症的发生情况.结果 与IB组比较,HB组麻醉平面达T_8～T_(10)时收缩压升高,布比卡因用量减少,患肢的有效镇痛时间和有效运动阻滞时间缩短,不良反应减少(P<0.01).两组术后均见未并发症发生.结论 轻比重布比卡因单侧连续腰麻用于老年患者全髋关节置换术麻醉平面可控性好,血液动力学稳定,不良反应少.     

Fentanyl shows different effects by administration routes on bispectral index during spinal anesthesia in patients undergoing cesarean section

BACKGROUND: Spinal anesthesia using a local anesthetic with fentanyl has been reported to induce sedation. We previously reported that the bispectral index (BIS) value was significantly decreased by spinal anesthesia using only bupivacaine and fetanyl after cesarean delivery. In the present study, we studied the effect of different fentanyl administration routes on BIS values during spinal anesthesia for cesarean section. METHODS: Forty-six women scheduled for cesarean section were allocated into five-groups according to the route of fentanyl administration and amount of local anesthetic: intrathecal 0.5% isobaric bupivacaine 2.5 ml plus fentanyl 20 microg (n = 11), intrathecal 0.5% isobaric bupivacaine 2.5 ml plus intravenous fentanyl 100 microg (n = 12), intrathecal 0.5% isobaric bupivacaine 2.5 ml plus epidural fentanyl 100 microg (n = 8), intrathecal 0.5% isobaric bupivacaine 2.5 ml (n = 8), and intrathecal 0.5% isobaric bupivacaine 3.0 ml (n = 7). BIS values were recorded during anesthesia. RESULTS: BIS values in intrathecal fentanyl group were lower than those of other groups (P = 0.03). The cumulative duration of BIS values 80 and below 80 was longer in the intrathecal fentanyl group than those of other groups (P = 0.004). CONCLUSION: The BIS value was significantly decreased only by intrathecal fentanyl for cesarean section.     

Cyclosporin A has a protective effect with induced upregulation of Hsp70 and nNOS on severe spinal cord ischemic injury in rabbits.

The purpose of this study is to ascertain the neuroprotective effect of cyclosporin A on the 25-min surgical ischemia model in the spinal cords of rabbits with neuropathological correlation and histoimmunochemical analyses measuring HSP70 and neuronal NOS (nNOS). New Zealand white rabbits were randomly divided into four groups (each n = 8): the C2, C7, Cs2, and Cs7 groups. The C2 and C7 groups underwent a 25-min surgical aortic cross-clamp without intervention and were sacrificed respectively on day 2 and on day 7 postoperatively. The Cs2 and Cs7 groups received cyclosporin A (25 mg/kg) intravenously 15 min after the 25-min cross-clamp and were sacrificed respectively on day 2 and day 7 postoperatively. Neurologic functions were evaluated on postoperative days 2 and 7 using the Tarlov scoring system. Then the rabbits were sacrificed for histopathologic observation. HSP 70 and nNOS stains with TUNEL assay were done for the C2 and Cs2 groups. All rabbits survived the experimental procedure. Tarlov's score for the Cs7 group (2.75 +/- 0.89) was significantly higher than that of the C7 group (1.25 +/- 1.39) (p < .05). Tarlov's score of the Cs7 group was also statistically higher on day 7 than on day 2 (p < .05). Strong correlation between the neurological and histological scorings was found. The TUNEL assay showed that the mean number of positive cells in the C2 group was 17.5 +/- 22.6 and in the Cs2 group was 12.5 +/- 11.1, but there was no statistically significant difference between the groups. There was more expression of HSP70 and nNOS in the cyclosporin groups than in the ischemia groups. In conclusion, this study demonstrates that cyclosporin A reduces neurological injury in the rabbit model of 25-min spinal cord ischemia. The neuroprotective effect of cyclosporin A against ischemia seems to be related to overexpressions of nNOS and HSP70.     

Neurologic and histopathologic evaluation after high-volume intrathecal amitriptyline

BACKGROUND AND OBJECTIVES: Accumulating evidence indicates that amitriptyline decreases pain sensation when administered orally, intraperitoneally, or for sciatic nerve block. Previous reports of intrathecal administration of amitriptyline have yielded inconsistent results. The failure of amitriptyline to provide antinociception may partly be related to its high logP (octanol-water partition coefficient) and consequent poor spread within the cerebrospinal fluid. We evaluated spinal block after various concentrations of amitriptyline administered intrathecally in a fixed high volume. METHODS: We administered 100 microL of 5, 10, 15.9 (0.5%), 25, 50, or 100 mmol/L amitriptyline hydrochloride solution or 100 microL of 15.4 mmol/L (0.5%) bupivacaine hydrochloride solution intrathecally to rats. The neurologic deficit was evaluated by antinociceptive, motor, and proprioceptive responses, and the spinal cord was examined for histopathologic changes. RESULTS: Doses of 100 microL amitriptyline at 15.9 mmol/L (0.5%) and 25 mmol/L produced longer complete nerve block than did bupivacaine at 15.4 mmol/L (0.5%); 5 and 10 mmol/L amitriptyline produced only partial nerve block. However, with 100 microL intrathecal amitriptyline at 50 and 100 mmol/L, many rats did not fully recover from spinal block. Severe axonal degeneration, myelin breakdown, and replacement of neuronal structures by vacuoles were seen in the spinal root section of animals injected with concentrations higher than 25 mmol/L amitriptyline. CONCLUSIONS: At lower doses, intrathecal injection of high volumes of amitriptyline results in long-acting spinal block. At higher doses, intrathecal amitriptyline results in irreversible neurologic deficit. Therefore, we do not recommend the use of intrathecal amitriptyline because of a very low therapeutic index.     

Protective effect of intrathecal ketorolac in spinal cord ischemia in rats: a microdialysis study

BACKGROUND: The prevention of ischemic paraplegia after thoracoabdominal aortic surgery is challenging for both anesthesiologists and surgeons. In a previous study, we showed that intrathecal ketorolac pre-treatment protects rats against ischemic spinal cord injury. In the present study, using a microdialysis method, we investigated whether this neuroprotective effect was related to changes in the spinal cord release of nitric oxide (NO) or the excitatory amino acids (EAAs) aspartate and glutamate. METHODS: Rats were randomized to receive either intrathecal saline or ketorolac 60 microg (10 rats per group), 1 h before spinal cord ischemic injury induced by balloon inflation of a 2F Fogarty catheter in the thoracic aorta with maintenance of the proximal arterial blood pressure at 40 mmHg for 11 min, followed by reperfusion. Another 10 animals were used as the sham-operated control group. Ischemic injury was assessed by hind limb motor function. Cerebrospinal fluid dialysates were collected at baseline (before ischemia) and at 1, 2, 3, 4, 6, 12 and 24 h after the start of reperfusion, and were analyzed for EAAs using high-performance liquid chromatography and for NO metabolites using an NO analyzer. RESULTS: The results showed that intrathecal ketorolac attenuated spinal cord ischemic injury. Dialysate concentrations of NO and EAAs were increased after spinal cord ischemia, and this effect was inhibited by intrathecal administration of ketorolac. CONCLUSIONS: The results of this study suggest that the neuroprotective effect of intrathecal ketorolac in spinal cord ischemia in rats may be caused by a decrease in the spinal cord release of NO and EAAs.     

Intrathecal bupivacaine protects against extension of lesions in an acute photochemical spinal cord injury model

PURPOSE: The photochemical spinal-cord injury model reproduces extensive secondary lesions that occur after spinal injury. We have evaluated in 27 rats the functional, electrophysiological and anatomical consequences of a photochemical spinal-cord lesion induced before or after intrathecal injection of bupivacaine. METHODS: After randomization, nine rats received 20 micro L of intrathecal bupivacaine 0.5% 15 min before a photochemical spinal-cord lesion (Group I) and eight rats received 20 micro L intrathecal bupivacaine 15 min after such a lesion (Group II). Ten rats received 20 micro L of saline 15 min before the photochemical injury (control group). Paraplegia was tested on days one, three, five, seven, nine, 12, 15 and 18 using an evaluation of hindlimb movements and an inclined plane stability test. Sensory block was evaluated by the animal's response when each hindlimb was brought into contact with a hot plate. Sympathetic injury was evaluated in terms of bladder voiding dysfunction. On day 18, residual somatosensory evoked potentials (SEP) were measured and the area of the intact spinal cord was determined using a digitalized system. RESULTS: Early paraplegia recovery was found in the two bupivacaine groups (P < 0.05). On day 12, motor recovery was complete in both bupivacaine groups whereas recovery was not complete on day 18 in the control group. Compared to the control group, inclined plane stability recovered earlier in Groups I and II, from day three to day 15. Sensory and sympathetic block scores were not different in the three groups. Nevertheless, SEP latencies were longer and amplitudes were lower in control group rats compared with the two bupivacaine groups on day 18. The intact spinal-cord cross-sectional area around the lesion was not different in the three groups. CONCLUSION: Twenty microlitres of intrathecal bupivacaine before or after acute photochemical spinal injury improves hindlimb motor recovery and SEP parameters in rats.     

Effects of xenon on ischemic spinal cord injury in rabbits: a comparison with propofol

Background: Xenon has been shown to reduce cellular injury after cerebral ischemia. However, the neuroprotective effects of xenon on ischemic spinal cord are unknown. The authors compared the effects of xenon and propofol on spinal cord injury following spinal cord ischemia in rabbits. Methods: Thirty‐two male New Zealand white rabbits were randomly assigned to one of three groups. In the xenon and propofol group, 70% of xenon and 0.8 mg/kg/min of propofol were administered 30 min before an aortic occlusion and maintained until the end of the procedure. The aortic occlusion was performed for 15 min. In the sham group, the aorta was not occluded. After an assessment of the hind limb motor function using the Tarlov score (0=paraplegia, 4=normal) at 48 h after reperfusion, gray and white matter injuries were evaluated based on the number of normal neurons in the anterior spinal cord and the percentage areas of vacuolation in the white matter, respectively. Results: In the xenon and propofol groups, the Tarlov score and the number of normal neurons were significantly lower than those in the sham group, whereas the percentage areas of vacuolation were similar among the three groups. There were no significant differences in Tarlov scores and the number of normal neurons between the xenon and the propofol groups. Conclusion: The results indicated that 70% of xenon has no additional neuroprotective effects on ischemic spinal cord injury in rabbits compared with propofol.     

Subarachnoid sufentanil as sole agent vs standard spinal bupivacaine in transurethral resection of the bladder

AIM: The aim of the study was to determine whether intrathecal sufentanil alone provides an adequate analgesia for patients undergoing transurethral resection of the bladder (TURB) and to compare it to standard spinal bupivacaine anesthesia in terms of motor and sensory blockade, discharge time and side effects. METHODS: Sixty-two patients were blindly and randomly assigned to receive either intrathecal bupivacaine (10 mg of 0.5% hyperbaric bupivacaine) or intrathecal sufentanil (15 microg). Motor and sensory blockade was evaluated using a modified Bromage scale as well as cold and pinprick tests. Severity of pain was assessed by means of a 10-point verbal analog scale. RESULTS: We found that the mean duration of sensory blockade was similar for both sufentanil and bupivacaine patients but the quality of analgesia induced by sufentanil alone was poor as compared with spinal bupivacaine anesthesia. CONCLUSION: The subarachnoid administration of sufentanil 15 mg seems to be inadequate for TURB surgery. In addition, the advantage of a faster recovery we observed in sufentanil patients is minimized by the occurrence of a troublesome symptom such as pruritus. On the other hand, spinal bupivacaine produces an undesirable motor blockade exceeding, in our opinion, the requirement for TURB procedure.     

Intrathecal clonidine added to small-dose bupivacaine prolongs postoperative analgesia in patients undergoing transurethral surgery

Introduction:

The aim of this prospective, double-blinded study was to investigate the effects of clonidine in co-administration with bupivacaine during spinal anesthesia, regarding the onset and regression of motor and sensory block, postoperative analgesia and possible side effects.

Methods:

We randomly selected 66 male patients (age 35 to 70), from the American Society of Anesthesiologists (ASA) class I–II; these patients were scheduled for transurethral surgical procedures. These patients were randomly allocated into two groups of 33 patients each: group B (bupivacaine) only received 0.5% isobaric bupivacaine 7.5 mg intrathecally and group BC (bupivacaine + clonidine) received bupivacaine 7.5 mg and clonidine 25 μg intrathecally. We performed the spinal anesthesia at a level of L3–L4 with a 25-gauge needle. We assessed the sensory block with a pin-prick, the motor block using the Bromage scale, analgesia with the visual analog scale and sedation with the modified Wilson scale. We also recorded the hemodynamic and respiratory parameters.

Results:

The groups were demographically similar. The mean time of achievement of motor block (Bromage 3) and sensory block at level T9 was significantly shorter in the BC group compared with B group (p = 0.002, p = 0.000, respeectively). The motor block regression time was not significantly different between the two groups (p = 0.237). The postoperative analgesia requirement was significantly longer in group BC compared with group B (p = 0.000). No neurological deficit, sedation or other significant adverse effects were recorded.

Conclusion:

The intrathecal application of clonidine in combination with bupivacaine improves the duration and quality of spinal anesthesia; it also provides longer duration of postoperative analgesia, without significant side effects.     

Intrathecal low-dose bupivacaine versus lidocaine for in vitro fertilization procedures

BACKGROUND AND OBJECTIVES: Recent controversy with the use of intrathecal lidocaine has prompted the search for suitable ambulatory surgery alternatives. The purpose of our study was to evaluate the clinical utility of intrathecal low-dose bupivacaine for outpatient transvaginal oocyte retrieval. METHODS: Forty women enrolled and completed our prospective, randomized, double-blinded study of intrathecal hyperbaric bupivacaine 3.75 mg (0.5 mL of 0.75%) with fentanyl 25 microg versus hyperbaric lidocaine 30 mg (2.0 mL of 1.5%) with fentanyl 25 microg. Onset and level of sensory and motor block; time to ambulation, urination, and discharge; and intra- and postoperative complications (hypotension, pruritus, nausea, emesis, postdural puncture headache, post spinal pain syndrome [PSPS]) were recorded. Data were evaluated using analysis of variance, chi-squared, and Mann-Whitney U tests, with P <.05 considered significant. RESULTS: In demographically similar groups, no differences were noted in times to onset and recovery of sensory and motor function, or complications; however, times to voiding and discharge were significantly longer in the bupivacaine group. Four and 2 patients in the bupivacaine and lidocaine groups, respectively, required intravenous analgesic supplementation. One patient in the lidocaine group experienced PSPS. CONCLUSIONS: Although prolongation to voiding and discharge was observed, intrathecal hyperbaric bupivacaine 3.75 mg with fentanyl 25 microg is a viable anesthetic for oocyte retrieval.