Evaluation of endometrial cytology: cytohistological correlations in 1,441 cancer patients.

BACKGROUND: Endometrial cytology by direct intrauterine sampling is the most common test for an initial evaluation of the endometrium in Japan. However, its diagnostic value for endometrial cancer remains unknown. Here, we assess the correlation between cytopathology and histopathology to evaluate the diagnostic value of cytology for endometrial cancer. METHODS: Patients with histologically confirmed endometrial cancer and controls with a normal endometrium confirmed by hysterectomy had all undergone preoperative endometrial cytology between 2001 and 2010 at our eight institutions and were retrospectively analyzed. The cytological results were compared by clinical stage, histological type, differentiation, and sampling instrument. RESULTS: We analyzed 1,441 endometrial cancer and 1,361 control cases. Endometrial cytology detected cancer in 1,279 (916 positive and 363 suspicious) cases with a sensitivity (positive plus suspicious cases) of 88.8% and a specificity of 98.5%. The positive rate was high in advanced-stage, nonendometrioid, and undifferentiated cases, but there was no significant difference in sensitivity between these clinical conditions. CONCLUSION: Endometrial cytology shows a relatively high sensitivity and specificity for endometrial cancer, and neither statistical measure is significantly affected by clinical stage, histological type, differentiation, sample numbers, or sampling instrument. These findings form a superior dataset for evaluating the efficacy of endometrial cytology.

Catalog of 525 sprites observed over Japan from September 2016 to March 2021.

We present a catalog of 525 sprites detected over the Sea of Japan and a northeast part of the Pacific Ocean from Sagamihara between September 2016 and March 2021. We analyze the morphology of 525, estimate the location of 441, and calculate the accurate top height of 15 sprites. More than half of our samples occurred in winter, while only 11% were in summer. In terms of morphology, 52% to 60% column type sprites took place in spring, autumn, and winter, while only 15.5% in summer. Therefore, summer thunderstorms are more likely to produce sprites with complex structures like carrots. Furthermore, sprites in summer are almost all located on the main island of Japan, and their spatial distributions are significantly different from the other seasons. Finally, from the perspective of the time distribution, the number of sprites is the largest at 1:00 JST. In addition, the morphology of sprites tends to be simple (e.g., a column type) at midnight JST.

[A case of deep vein thrombosis in spite of using an intermittent pneumatic compression device].

A 69-year-old male patient underwent subtotal esophagectomy for esophageal cancer under sevoflurane anesthesia combined with epidural analgesia. According to the protocol for the prevention of deep vein thrombosis (DVT) in our hospital, only an intermittent pneumatic compression device (IPC) and elastic stockings were perioperatively used for prophylaxis of DVT although D-dimer level was slightly increased to 1.2 microg x ml(-1). On the 2nd post-operative day, a venous ultrasound examination was performed, because D-dimer level was suddenly increased up to 41.5 microg x ml(-1) without any signs of thrombus in the atrium and pleural cavity. Since DVT was detected with the right lower limb, the use of an IPC was stopped and an inferior vena cava filter was inserted through the right jugular vein with a continuous administration of heparin. An aggressive search should be performed if DVT is suspected by any clinical signs including an increase in D-dimer level. We should also keep in mind the possibility of DVT even if an IPC and elastic stockings are perioperatively used.

Jugular bulb oxygen saturation under propofol or sevoflurane/nitrous oxide anesthesia during deliberate mild hypothermia in neurosurgical patients.

Sevoflurane and propofol have been widely used as anesthetic agents for neurosurgery. Recent evidence has suggested that the influence of these anesthetics on cerebral oxygenation may differ. In the present study, the authors investigated jugular bulb oxygen saturation (SjO2) during propofol and sevoflurane/nitrous oxide anesthesia under mildly hypothermic conditions. After institutional approval and informed consent, 20 patients undergoing elective craniotomy were studied. Patients were randomly divided to the group S/N2O (sevoflurane/nitrous oxide/fentanyl anesthesia) or the group P (propofol/fentanyl anesthesia). After induction of anesthesia, the catheter was inserted retrograde into the jugular bulb and SjO2 was analyzed. During the operation, patients were cooled and tympanic membrane temperature was maintained at 34.5 degrees C. SjO2 was measured at normocapnia during mild hypothermia and at hypocapnia during mild hypothermia. There were no statistically significant differences in demographic variables between the groups. During mild hypothermia, SjO2 values were significantly lower in group P than in group S/N2O. The incidence of SjO2 less than 50% under mild hypothermic-hypocapnic conditions was significantly higher in group P than in group S/N2O. These results suggest that hyperventilation should be more cautiously applied during mild hypothermia in patients anesthetized with propofol and fentanyl versus sevoflurane/nitrous oxide/fentanyl.

Amplitudes and intrapatient variability of myogenic motor evoked potentials to transcranial electrical stimulation during ketamine/N2O- and propofol/N2O-based anesthesia.

The aim of the current study was to investigate whether there are differences in amplitudes and intrapatient variability of motor evoked potentials to five pulses of transcranial electrical stimulation between ketamine/N2O- and propofol/N2O-based anesthesia. Patients in the propofol group (n = 13) and the ketamine group (n = 13) were anesthetized with 50% N2O in oxygen, fentanyl, and 4 mg/kg/hr of propofol or 1 mg/kg/hr of ketamine, respectively. The level of neuromuscular blockade was maintained at an M-response amplitude of approximately 50% of control. Motor evoked potentials in response to multipulse transcranial electrical stimulation were recorded from the right adductor pollicis brevis muscle, and peak-to-peak amplitude and onset latency of motor evoked potentials were evaluated. To estimate intrapatient variability, the coefficient of variation (standard deviation/mean x 100%) of 24 consecutive responses was determined. Motor evoked potential amplitudes in the ketamine group were significantly larger than in the propofol group (mean, 10th-90th percentile: 380 microV, 129-953 microV; 135 microV, 38-658 microV, respectively; P <.05). There were no significant differences in motor evoked potential latency (mean +/- standard deviation: 20.9 +/- 2.2 msec and 21.4 +/- 2.2 msec, respectively) and coefficient of variation of amplitudes (median [range]: 32% [22-42%] and 26% [18-41%], respectively) and latencies (mean +/- standard deviation: 2.1 +/- 0.7% and 2.1 +/- 0.7%, respectively) between the ketamine and propofol groups. In conclusion, intrapatient variability of motor evoked potentials to multipulse transcranial stimulation is similar between ketamine/N2O- and propofol/N2O-based anesthesia, although motor evoked potential amplitudes are lower during propofol/N2O-based anesthesia than ketamine/N2O-based anesthesia.

Long-term assessment of hind limb motor function and neuronal injury following spinal cord ischemia in rats.

Recent evidence suggests that brain injury caused by ischemia is a dynamic process characterized by ongoing neuronal loss for at least 14 days after ischemia. However, long-term outcome following spinal cord ischemia has not been extensively examined. Therefore, we investigated the changes of hind limb motor function and neuronal injury during a 14-day recovery period after spinal cord ischemia. Male Sprague-Dawley rats received spinal cord ischemia (n = 64) or sham operation (n = 21). Spinal cord ischemia was induced by inflation of a 2F Fogarty catheter placed into the thoracic aorta for 6, 8, or 10 minutes. The rats were killed 2, 7, or 14 days after reperfusion. Hind limb motor function was assessed with the 21-point Basso, Beattie, and Bresnahan (BBB) scale during the recovery period. The number of normal and necrotic neurons was counted in spinal cord sections stained with hematoxylin/eosin. Longer duration of spinal cord ischemia produced severer hind limb motor dysfunction at each time point. However, BBB scores gradually improved during the 14-day recovery period. Neurologic deterioration was not observed between 7 and 14 days after reperfusion. The number of necrotic neurons peaked 2 days after reperfusion and then decreased. A small number of necrotic neurons were still observed 7 and 14 days after reperfusion in some of the animals. These results indicate that, although hind limb motor function may gradually recover, neuronal loss can be ongoing for 14 days after spinal cord ischemia.

[Sevoflurane can induce rhabdomyolysis in Duchenne's muscular dystrophy].

Rhabdomyolysis is one of the perioperative complications in patients with Duchenne's muscular dystrophy (DMD). It has been suggested that sevoflurane can be used safely for anesthesia in patients with DMD. In this report, we describe a case with DMD who received anesthesia with sevoflurane, in which rhabdomyolysis developed postoperatively. A 6-year-old boy diagnosed as DMD was scheduled for tonsillectomy under general anesthesia. Preoperative laboratory examination revealed a high level of creatine kinase (CK) (16,000-32,000 IU.l-1). An abnormality of the dystrophin gene was detected by DNA analysis. Anesthesia was induced with sevoflurane without muscle relaxant, and maintained with sevoflurane in nitrous oxide and oxygen under controlled ventilation. The course of anesthesia was uneventful and the patient recovered smoothly. Three hours postoperatively, dark red urine with a high concentration of myoglobin (1,390,000 ng.ml-1) was recognized with a high level of CK (63,500 IU.l-1). Body temperature was 37.6 degrees C, and electrocardiogram and serum potassium were within normal ranges. After the diuresis with mannitol and furosemide, the urine became clear. On the 4th postoperative day, he was discharged without any complication. This case suggested that rhabdomyolysis can develop after sevoflurane anesthesia in patients with DMD.

Effects of delta-opioid agonist SNC80 on white matter injury following spinal cord ischemia in normothermic and mildly hypothermic rats.

PURPOSE: Although the delta-opioid agonist SNC80 has been shown to attenuate hind-limb motor function and gray matter injury in normothermic rats subjected to spinal cord ischemia (SCI), its effects on white matter injury remain undetermined. In the present study, we investigated whether SNC80 could attenuate white matter injury in normothermic and mildly hypothermic rats. METHODS: Forty rats were randomly allocated to one of following five groups: vehicle or SNC80 with 10 min of SCI at 38 degrees C (V-38-10m or SNC-38-10m, respectively), vehicle or SNC80 with 22 min of SCI at 35 degrees C (V-35-22m or SNC-35-22m, respectively), or sham. SNC80 or vehicle was intrathecally administered 15 min before SCI. Forty-eight hours after reperfusion, the white matter injury was evaluated by the extent of vacuolation. RESULTS: The percent area of vacuolation in the ventral white matter was significantly lower in the SNC-38-10m and SNC-35-22m groups compared with that in the V-38-10m and V-35-22m groups, respectively (P < 0.05). CONCLUSION: The results indicate that intrathecal treatment with the delta-opioid agonist SNC80 can attenuate the ventral white matter injury following SCI in rats under normothermic and mildly hypothermic conditions.

Telomerase expression and cell proliferation in ovarian cancer cells induced by histone deacetylase inhibitors.

OBJECTIVE: Telomerase is composed primarily of catalytic subunit (hTERT) and RNA template (hTERC). Histone deacetylase (HDAC) inhibitors are known to modulate transcription and change the expression of hTERT and hTERC mRNA and telomerase activity in several types of cancer cells, but it is unclear if there is a similar effect in ovarian cancer cells. METHOD: The present study was designed to evaluate the effects of HDAC inhibitors on hTERT and hTERC mRNA expression in ovarian cancer cells. SK-V-3 cells were treated with the HDAC inhibitors, trichostatinA (TSA) and sodium butyrate (NaB); the expression of hTERC and hTERT mRNA and telomerase activity were evaluated by RT-PCR and TRAP assay, respectively. RESULTS: In SK-OV-3 cells, TSA and NaB inhibited cell proliferation and induced apoptosis. The expression of hTERT and hTERT mRNA was not suppressed even after treatment with 1.0 microM TSA and 6 mM NaB, respectively. The telomerase activity was not changed by either TSA or NaB. CONCLUSION: Histone deacetylase inhibitors inhibited cell proliferation and induced apoptosis, but had no effect on the expression of hTERC and hTERT mRNA and on telomerase activity.

An evaluation of white matter injury after spinal cord ischemia in rats: a comparison with gray matter injury.

We quantitatively assessed both gray and white matter injury after spinal cord ischemia in rats, and the relationship between the magnitude of gray and white matter injury was determined. Twenty-five male rats were anesthetized with isoflurane, and spinal cord ischemia (SCI) was induced by balloon intraaortic occlusion combined with hypotension. The animals were randomly allocated to one of the following three groups: animals with SCI for 12 min (SCI-12; n = 8), 15 min (SCI-15; n = 9), or those with sham operation (n = 8). Twenty-four hours after reperfusion, hindlimb motor function was assessed using the Basso-Beattie-Bresnahan scale scoring. Gray matter damage was assessed on the basis of the number of normal neurons in the ventral horn. White matter damage was assessed on the basis of the extent of vacuolation and amyloid precursor protein immunoreactivity in the ventral and ventrolateral white matter. There were significantly less normal neurons in the SCI-15 group compared with those in the SCI-12 and sham groups (P < 0.05). There was a significant positive correlation between the Basso-Beattie-Bresnahan scores and the number of normal neurons. The percentages of vacuolation areas in the SCI-15 group were significantly larger compared with those in the SCI-12 and sham groups (30% +/- 10% versus 9% +/- 7%, 0% +/- 0%, P < 0.05). Immunohistochemical analysis revealed increased amyloid precursor protein immunoreactivity in the swollen axons, especially in the SCI-15 group. There was a significant negative correlation between the number of normal neurons and percentages of vacuolation areas. These results indicate that both gray and white matter were injured after SCI in rats and the degree of white mater injury was correlated with the severity of gray matter injury after a relatively short recovery period.

Effect of mild hypothermia on inodilator-induced vasodilation of pial arterioles in cats.

BACKGROUND: Mild hypothermia has been proposed as a means of providing cerebral protection after traumatic brain injury. However, hypothermia has been shown to alter not only physiologic but also pharmacologic responses. The purpose of this study was to investigate whether mild hypothermia (3-4 degrees C temperature reduction) could alter cerebral vasodilation induced by inodilators, which are characterized by having an inotropic effect in addition to a vasodilatory effect. Isoproterenol (a beta-adrenergic receptor agonist), colforsin dapropate (an adenylate cyclase stimulant), and amrinone (a phosphodiesterase inhibitor) were chosen as inodilators. METHODS: The cranial window technique, combined with microscopic video recording, was used. Forty-eight cats were randomly assigned to either a normothermic or a hypothermic group (33 degrees C). Isoproterenol, colforsin dapropate, or amrinone was topically applied in the cranial window and the diameter of pial arterioles was measured. RESULTS: Topical administration of isoproterenol, colforsin dapropate, and amrinone produced a significant dilation in a dose-dependent manner during normothermia. The vasodilation induced by these inodilators was not affected by mild hypothermia. CONCLUSION: The vasodilation induced by topical administration of isoproterenol, colforsin dapropate, and amrinone was not affected by mild hypothermia.

The influence of induced hypothermia for hemostatic function on temperature-adjusted measurements in rabbits.

UNLABELLED: In hypothermic patients, a tendency to bleed may be observed even when hemostatic tests seem to be normal. Coagulation and platelet function tests are usually performed at 37 degrees C. We investigated the influence of induced hypothermia on temperature-adjusted hemostasis function testing using Sonoclot Analyzer (Sonoclot) and Thromboelastography (TEG). Anesthesia was induced and maintained with IV ketamine and fentanyl on 15 male New-Zealand White rabbits. A water blanket was used to induce hypothermia to 30 degrees C and to rewarm to 37 degrees C. Blood samples were obtained at four points: before hypothermia, at 34 degrees C, at 30 degrees C, and after rewarming. Standard coagulation tests were performed at 37 degrees C (C method), and simultaneously, real temperature hemostasis function tests (R method) were run. In Sonoclot(R), activated clotting time and time to peak increased and clot rate decreased significantly at 30 degrees C in the R method compared with those in the C method. In TEG(R), reaction time and clot formation time were prolonged and clot formation rate was diminished at 30 degrees C in the R method compared with those in the C method. Induced hypothermia delayed the coagulation cascade and reduced platelet function. During hypothermia, hemostatic measurements should be performed at real temperature to avoid overestimating patient hemostatic function based on results measured at the standard 37 degrees C. IMPLICATIONS: We investigated the influence of induced hypothermia on temperature-adjusted hemostasis function tests in rabbits using Sonoclot Analyzer and Thromboelastography. Induced hypothermia delayed the coagulation cascade and reduced platelet function. The conventional coagulation tests performed at 37 degrees C failed to detect these hypothermia-induced degradations in hemostasis performance.

The effect of hypothermia on myogenic motor-evoked potentials to electrical stimulation with a single pulse and a train of pulses under propofol/ketamine/fentanyl anesthesia in rabbits.

UNLABELLED: In the present study, we investigated the effect of hypothermia on myogenic motor-evoked potentials (MEPs) in rabbits. The influence of stimulation paradigms to induce MEPs was evaluated. Twelve rabbits anesthetized with ketamine, fentanyl, and propofol were used for the study. Myogenic MEPs in response to electrical stimulation of the motor cortex with a single pulse and a train of three and five pulses were recorded from the soleus muscle. After the control recording of MEPs at 38 degrees C of esophageal temperature, the rabbits were cooled by surface cooling. Esophageal temperature was maintained at 35 degrees C, 32 degrees C, 30 degrees C, and 28 degrees C, and MEPs were recorded at each point. MEP amplitude to single- pulse stimulation was significantly reduced with a re-duction of core temperature to 28 degrees C compared with the control value at 38 degrees C (0.8 +/- 0.4 mV versus 2.3 +/- 0.3 mV; P < 0.05), whereas MEP amplitude to train-pulse stimulation did not change significantly during the cooling. MEP latency was increased linearly with a reduction of core temperature regardless of stimulation paradigms. In conclusion, these results indicate that a reduction of core temperature to 28 degrees C did not influence MEP amplitudes as long as a train of pulses, but not a single pulse, was used for stimulation in rabbits under propofol/ketamine/fentanyl anesthesia. IMPLICATIONS: Intraoperative monitoring of myogenic motor-evoked potentials (MEPs) may be required under hypothermic conditions because of its neuroprotective efficacy. However, data on the influence of hypothermia on myogenic MEPs are limited. The results indicate that multipulse stimulation may be better than single-pulse stimulation when monitoring MEPs during hypothermia.

Evaluation of rapid ischemic preconditioning in a rabbit model of spinal cord ischemia.

BACKGROUND: Rapid ischemic preconditioning (IPC) has been shown to reduce cellular injury after subsequent cardiac and cerebral ischemia. However, the data on rapid IPC of the spinal cord is limited. The authors investigated whether pretreatment with sublethal ischemia of spinal cord can attenuate neuronal injury after spinal cord ischemia in rabbits. METHODS: Forty-seven male New Zealand white rabbits were randomly assigned to one of three groups (n = 15 or 16 each). In the IPC(-) group, the infrarenal aorta was occluded for 17 min to produce spinal cord ischemia. In the IPC(+) group, 5 min of aortic occlusion was performed 30 min before 17 min of spinal cord ischemia. In the sham group, the aorta was not occluded. Hind limb motor function was assessed at 3 h, 24 h, 4 days, and 7 days after reperfusion using Tarlov scoring (0 = paraplegia; 4 = normal). Animals were killed for histopathologic evaluation at 24 h or 7 days after reperfusion. The number of normal neurons in the anterior spinal cord (L4-L6) was counted. RESULTS: Neurologic scores were significantly higher in the IPC(+) group than the IPC(-) group at 3 and 24 h after reperfusion (P < 0.05). However, neurologic scores in the IPC(+) group gradually decreased and became similar to those in the IPC(-) group at 4 and 7 days after reperfusion. At 24 h after reperfusion, the numbers of normal neurons were significantly higher in the IPC (+) group than in the IPC(-) group (P < 0.05) and were similar between the IPC(+) and sham groups. At 7 days after reperfusion, there was no difference in the number of normal neurons between the IPC(+) and IPC(-) groups. CONCLUSION: The results indicate that rapid IPC protects the spinal cord against neuronal damage 24 h but not 7 days after reperfusion in a rabbit model of spinal cord ischemia, suggesting that the efficacy of rapid IPC may be transient.

High-dose amrinone is required to accelerate rewarming from deliberate mild intraoperative hypothermia for neurosurgical procedures.

BACKGROUND: Since the time available to provide the cooling and rewarming is limited during deliberate mild hypothermia, the technique to accelerate the cooling and rewarming rate of core temperature has been studied. Amrinone has been reported to accelerate the cooling rate but not the rewarming rate of core temperature during deliberate mild hypothermia. The failure of amrinone effect on the rewarming rate might be due to an insufficient dose of amrinone during hypothermic conditions. The authors therefore tested whether higher doses of amrinone can accelerate the rewarming rate of core temperature during deliberate mild hypothermia for neurosurgery. METHODS: After institutional approval and informed consent, 30 patients were randomly assigned to one of three groups. Patients in the control group (n = 10) did not receive amrinone; patients in the AMR 15 group (n = 10) received 15 microg x kg(-1) x min(-1) amrinone with a 1.0-mg/kg loading dose of amrinone at the beginning of cooling; and patients in the ReAMR group (n = 10) received 5 microg x kg(-1) x min(-1) amrinone with 1.0-mg/kg loading and reloading doses of amrinone at the beginning of cooling and rewarming, respectively. Administration of amrinone was started just after the induction of cooling and continued until the end of anesthesia. Anesthesia was maintained with nitrous oxide in oxygen, propofol, and fentanyl. After induction of anesthesia, patients were cooled, and tympanic membrane temperature was maintained at 34.5 degrees C. After completion of the main surgical procedures, patients were actively rewarmed and extubated in the operating room. RESULTS: The cooling and rewarming rates of core temperature were both significantly faster in both amrinone groups than in the control group. During the cooling and rewarming periods, forearm minus fingertip temperature gradient was significantly smaller in both amrinone groups than in the control group. During the rewarming period, heart rate and mean arterial pressure in the AMR 15 group were significantly faster and lower, respectively, than in the control group. Systemic vascular resistance in the AMR 15 group was smaller than in the control group throughout the study; on the other hand, only the value after the start of rewarming in the ReAMR group was smaller than in the control group. CONCLUSIONS: Amrinone at an infusion rate of 15 or 5 microg x kg(-1) x min(-1) with a reloading at the beginning of rewarming accelerated the rewarming rate of core temperature during deliberate mild hypothermia. This suggests that high-dose amrinone is required to accelerate rewarming from deliberate mild intraoperative hypothermia for neurosurgical procedures.

Intraoperative monitoring of myogenic motor-evoked potentials from the external anal sphincter muscle to transcranial electrical stimulation.

STUDY DESIGN: Motor-evoked potentials from the external anal sphincter were analyzed using transcranial electrical stimulation during spinal surgery in patients under general anesthesia. OBJECTIVE: To investigate whether motor-evoked potentials from the external anal sphincter could be elicited by transcranial electrical stimulation under general anesthesia. SUMMARY OF BACKGROUND DATA: Lumbosacral surgery often places nerve rootlets at risk for injury during operative dissection. Specifically, injury for sacral rootlets can result in bowel and bladder dysfunction, but the techniques for monitoring bowel and bladder function are limited. METHODS: Thirty patients who underwent elective spinal surgery were studied. Patients were anesthetized with 50% nitrous oxide in oxygen, fentanyl, and 4 mg/kg/h of propofol (n = 19) or 1 mg/kg/h of ketamine (n = 11). The level of neuromuscular blockade, assessed by recording the M-response from the right abductor pollicis brevis muscle, was maintained at an M-response amplitude of 40-50% of control. Motor-evoked potentials in response to a multipulse transcranial electrical stimulation at stimulus sites of C3-C4 or Fz-Cz were recorded from the skin over the subcutaneous part of the external anal sphincter using a plug-type electrode probe. The success rate of motor-evoked potentials' recording and peak-to-peak amplitude and the onset latency of motor-evoked potentials were evaluated. RESULTS: Success rates of motor-evoked potentials from the external anal sphincter were 73% and 53% after transcranial stimulation at stimulus sites of C3-C4 and Cz-Fz, respectively. Amplitudes of motor-evoked potentials after C3-C4 stimulation were significantly greater than those after Cz-Fz stimulation. Motor-evoked potential latency from the external anal sphincter was 18.6 +/- 1.5 and 19.0 +/- 2.7 msec after C3-C4 and Cz-Fz stimulation, respectively. CONCLUSIONS: The results suggest that, using a transcranial multipulse stimulation, monitoring of motor-evoked potentials from the external anal sphincter is feasible during ketamine- and propofol-based anesthesia. However, further improvement of techniques would be required for intraoperative elicitation of motor-evoked potentials from the external anal sphincter.

Noxious stimuli do not modify myogenic motor evoked potentials by electrical stimulation during anesthesia with propofol-based anesthesia.

PURPOSE: To investigate whether motor evoked potentials (MEP) to transcranial electrical stimulation under constant blood propofol concentration are affected by the arousing effect of surgical noxious stimuli. METHODS: Twenty patients who underwent elective spinal surgery were studied. Patients were anesthetized with 50% nitrous oxide in oxygen, fentanyl, and propofol to maintain the bispectral index (BIS) score around 50. MEP in response to a multipulse transcranial electrical stimulation at stimulus sites of C3-C4 were recorded over the right abductor pollicis brevis muscle. Changes of peak-to-peak amplitude and onset latency of MEP, BIS score before and after surgical stimuli were evaluated. Propofol plasma concentration was measured at the same time points. RESULTS: Both MEP amplitude and latency did not change significantly after surgical stimuli although BIS increased significantly (48 +/- 6 to 58 +/- 5; P < 0.05). Plasma propofol concentration was maintained at the same level between the two measurement points (3.3 +/- 0.7 to 3.3 +/- 0.7 micro g*mL(-1)). There was no relation between BIS change and changes of MEP amplitude and latency, and propofol plasma concentration. CONCLUSION: MEP to the transcranial electrical stimulation under a constant and clinically appropriate blood propofol concentration are not affected by surgical noxious stimuli.

Mild hypothermia can enhance pial arteriolar vasodilation induced by isoflurane and sevoflurane in cats.

OBJECTIVE: Volatile anesthetics have been shown to dilate cerebral vessels. Recent evidence suggests that mild hypothermia can alter vascular reactivity of the cerebral vessels. However, the effect of mild hypothermia on volatile anesthetic-induced vasodilation of cerebral vessels is unknown. In the present study, we investigated the effect of mild hypothermia on pial arteriolar vasodilation induced by isoflurane and sevoflurane in cats. DESIGN: Prospective, randomized, experimental study with repeated measures. SETTING: Investigational animal laboratory. SUBJECTS: Forty cats were used for the study of systemic administration of volatile anesthetics, and 22 cats were used for the study of topical administration of volatile anesthetics. INTERVENTIONS: This study was approved by the Animal Experiment Committee of Nara Medical University. Animals were anesthetized with pentobarbital to maintain suppressive electroencephalographic patterns, which were introduced to measure direct effects of anesthetic agents after removing metabolic effects. The cranial window technique, combined with microscopic video recording, was used for the measurement of small (50-100 microm) and large (100-200 microm) pial arteriolar diameter in an experiment. Animals were randomly assigned to either a normothermic (37 degrees C) or a hypothermic group (33 degrees C). Desired temperatures were maintained by using a water blanket. In the first phase of the study, the effect of hypothermia on pial arteriolar vasodilation induced by systemic administration of isoflurane or sevoflurane was assessed. Each cat received isoflurane or sevoflurane at 0.5, 1.0, 1.5, and 2.0 minimum alveolar anesthetic concentrations, and the diameter of pial arterioles was measured. In the second group of animals, the direct effect of isoflurane and sevoflurane on pial vessels was evaluated. The artificial cerebrospinal fluid bubbled with isoflurane or sevoflurane (minimum alveolar anesthetic concentrations of 1 or 3) was topically administered in the cranial window. MEASUREMENTS AND MAIN RESULTS: Systemic and topical administration of isoflurane and sevoflurane produced significant dilation of both small and large pial arterioles in a dose-dependent manner during normothermia. In the hypothermic group, vasodilation of small pial arterioles by systemic administration of isoflurane and sevoflurane at a high concentration was significantly larger than in the normothermic group (p <.05). Vasodilation of both small and large pial arterioles by topical administration of isoflurane and sevoflurane was significantly greater in the hypothermic group than in the normothermic group (p <.05). CONCLUSIONS: These results suggest that pial arteriolar vasodilation induced by isoflurane and sevoflurane can be enhanced by mild hypothermia in cats anesthetized with pentobarbital.

The effects of the delta-opioid agonist SNC80 on hind-limb motor function and neuronal injury after spinal cord ischemia in rats.

Recent investigation suggested neuroprotective efficacy of a delta-opioid agonist in the brain. We investigated the effects of intrathecal treatment with a delta-opioid agonist (SNC80) on spinal cord ischemia (SCI) in rats. SCI was induced with an intraaortic balloon catheter. The animals were randomly allocated to one of the following five groups: 1) SNC80 before 9 min of SCI (SNC-9; n = 12), 2) vehicle before 9 min of SCI (V-9; n = 12), 3) SNC80 before 11 min of SCI (SNC-11; n = 10), 4) vehicle before 11 min of SCI (V-11; n = 12), or 5) sham (n = 12). SNC80 (400 nmol) or vehicle was administered 15 min before SCI. Forty-eight hours after reperfusion, hind-limb motor function was assessed by using the Basso, Beattie, Bresnahan (BBB) scale (0 = paraplegia; 21 = normal) and histological assessment of the L4 and L5 spinal segments was performed. BBB scores in the SNC-9 group were higher compared with those in the V-9 group (P < 0.05), whereas there were no differences in BBB scores between the SNC-11 and V-11 groups. There were significantly more normal neurons in the SNC-9 and SNC-11 groups than in the V-9 and V-11 groups (P < 0.05). The results indicate that intrathecal treatment with the delta-opioid agonist SNC80 can attenuate hind-limb motor dysfunction and neuronal injury after SCI in rats.