Anesthesia and analgesia
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Anesthesia and analgesia · Mar 2004
Effect of isoflurane on neuronal apoptosis in rats subjected to focal cerebral ischemia.
Although isoflurane can reduce ischemic neuronal injury after short postischemic recovery intervals, this neuroprotective efficacy is not sustained. Neuronal apoptosis can contribute to the gradual increase in infarct size after ischemia. This suggests that isoflurane, although capable of reducing early neuronal death, may not inhibit ischemia-induced apoptosis. We investigated the effects of isoflurane on markers of apoptosis in rats subjected to focal ischemia. Fasted Wistar-Kyoto rats were anesthetized with isoflurane and randomly allocated to awake (n = 40) or isoflurane (n = 40) groups. Animals in both groups were subjected to focal ischemia by filament occlusion of the middle cerebral artery for 70 min. Pericranial temperature was servo-controlled at 37 degrees C +/- 0.2 degrees C throughout the experiment. In the awake group, isoflurane was discontinued and the animals were allowed to awaken. In the isoflurane group, isoflurane anesthesia was maintained at 1.5 MAC (minimum alveolar anesthetic concentration). Animals were killed 7 h, 1 day, 4 days, or 7 days after reperfusion (n = 10/group/time point). The area of cerebral infarction was measured by image analysis in a hematoxylin and eosin stained section. In three adjacent sections, apoptotic neurons were identified by TUNEL staining and immunostaining for active caspase-9 and caspase-3. Infarct size was smaller in the isoflurane group than the awake group 7 h, 1 day, and 4 days after reperfusion (P < 0.05). However, this difference was absent 7 days after reperfusion. The number of apoptotic (TUNEL, caspase-3, and caspase-9 positive) cells 1 day after ischemia was significantly more in the awake versus isoflurane group. After a recovery period of 4 or 7 days, the number of apoptotic cells in the isoflurane group was more than in the awake group. After 7 days, the number of caspase-3 and -9 positive neurons was more in the isoflurane group (P < 0.05). The data indicate that isoflurane delays but does not prevent the development of cerebral infarction caused by ischemia. Isoflurane reduced the development of apoptosis early after ischemia but did not prevent it at later stages of postischemic recovery. ⋯ The effect of isoflurane on neuronal apoptosis was investigated in rats subjected to focal cerebral ischemia. In isoflurane-anesthetized animals, ischemia-induced apoptosis occurred during the later stages of postischemic recovery. Isoflurane did not inhibit postischemic neuronal apoptosis.
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Anesthesia and analgesia · Mar 2004
Clinical TrialAssessing residual neuromuscular blockade using acceleromyography can be deceptive in postoperative awake patients.
Postoperative awake patients may have significant residual neuromuscular block. In awake patients, the results of accelerometry are affected by extra movements to which the thumb may be subject. In this study, we evaluated the repeatability of train-of-four (TOF) ratio using acceleromyography in 253 patients recovering from anesthesia. Immediately after arrival in the postanesthesia care unit, the ulnar nerve was stimulated with TOF stimulation. The evoked response at the thumb was measured by the TOF-Watch apparatus. The current intensity was 30 mA. Two TOF stimulations were applied and recorded at 30-s intervals. A Bland-Altman test was used. The Kappa (kappa) test for clinical agreement between the two measurements was also calculated according to the presence or absence of a residual neuromuscular blockade, defined as a TOF ratio <0.9. According to the presence of a residual neuromuscular blockade, the paired TOF ratios were discordant in 61 patients (24%; 95% confidence interval, 21%-27%). The kappa test indicated a moderate agreement (k = 0.47). We demonstrated that accelerometry as used in this study is not always accurate. Two isolated acceleromyograph TOF ratios are not an accurate representation of the neuromuscular status of the patient recovering from anesthesia. ⋯ Clinicians should be aware that acceleromyography as used in this study does not always provide precise train-of-four ratio measurements. Two isolated acceleromyograph train-of-four ratios are not an accurate representation of the neuromuscular status of the patient recovering from anesthesia.
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Anesthesia and analgesia · Mar 2004
Comparative StudyLocal anesthetic properties of a novel derivative, N-methyl doxepin, versus doxepin and bupivacaine.
Among various tricyclic antidepressants, doxepin and amitriptyline are also long-acting local anesthetics. We synthesized a new compound, N-methyl doxepin, and investigated whether this derivative possesses local anesthetic properties. N-methyl doxepin and doxepin were tested in a rat sciatic nerve model at 2.5, 5.0, and 10 mM. Proprioceptive, motor, and nociceptive blockade were evaluated and compared with those induced by 0.5% bupivacaine. Block of Na(+) channels by N-methyl doxepin and doxepin was assessed in cultured pituitary tumor cells under voltage clamp conditions. N-methyl doxepin elicited complete nociceptive blockade that generally lasted longer than that caused by doxepin (e.g., approximately 7.4 h versus 5.3 h at 10 mM). Significant differences were observed for full recovery of function at all concentrations and for the duration of complete blockade except at 2.5 mM. Bupivacaine at 0.5% (15.4 mM) was less effective in producing complete blockade (approximately 1.5 h) than N-methyl doxepin and doxepin. Both doxepin and N-methyl doxepin were potent Na(+) channel blockers, although N-methyl doxepin displayed a slower wash-in rate. No morphological alterations were detected in cross-sectioned sciatic nerve specimens with these three drugs. We conclude that N-methyl doxepin is a potent Na(+) channel blocker and a long-acting local anesthetic for rat sciatic nerve blockade. ⋯ N-methyl doxepin and doxepin are both potent Na(+) channel blockers; they elicit rat sciatic nerve block lasting longer than that induced by bupivacaine and seem to be nontoxic to peripheral nerves at concentrations up to 10 mM.
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Anesthesia and analgesia · Mar 2004
Case ReportsRetroperitoneal hematoma after spinal anesthesia with the paramedian approach.
We present a case of a patient who developed a retroperitoneal bleeding after spinal anesthesia using 22-gauge Quincke needle, with the paramedian approach. Two attempts were needed to accomplish the block. Four hours later the patient complained of back pain radiating to her left calf, with weakness of the quadriceps muscle. Computed tomography revealed a large retroperitoneal hematoma from bleeding lumbar artery. Angiography failed to demonstrate the vessel. The patient was transfused with packed red blood cells and recovered gradually. She had normal coagulation tests throughout the event. ⋯ We describe a case of a large retroperitoneal hematoma after the placement of an uneventful spinal block. The patient required four units of packed red blood cells despite having normal coagulation profiles throughout the event. The diagnosis and treatment of retroperitoneal hematoma are discussed.
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Anesthesia and analgesia · Mar 2004
Case ReportsArtifact in the bispectral index in a patient with severe ischemic brain injury.
The electroencephalogram (EEG) has been used to predict neurological outcome in patients with anoxic-ischemic brain injury. The bispectral index (BIS) may be a useful alternative. A persistently low BIS associated with burst-suppression of the raw EEG in the setting of minimal hypnotic drug administration may indicate severe cerebral ischemia. We report a case where a patient with presumed ischemic brain injury and an extremely low BIS had an unexplained increase in BIS that could be attributed to electrocardiogram artifact. Care should be taken when interpreting BIS in the setting of anoxic-ischemic brain injury or brain death. ⋯ The bispectral index (BIS) can be prone to artifact. In this report we found that electrocardiogram artifact led to an apparent normal BIS in a patient with complete burst-suppression associated with severe brain injury.