The effects of anesthetics on the generation of cortical spreading depression (CSD) were investigated. Volatile anesthetics halothane, isoflurane, sevoflurane (0.5, 1.0, and 2.0 MAC), and the intravenous anesthetic pentobarbital were studied. Cortical spreading depression was induced by 3M-KCl applied to a surface of brain cortex for 30 minutes. Direct current (DC) potential was recorded, and the number, amplitude, and duration of CSDs were observed. With increasing concentrations of each volatile anesthetic, there was a dose-related reduction in CSD frequency but not in CSD amplitude. At 2.0 MAC of sevoflurane the suppression of CSD was less than with the other volatile anesthetics. In addition, the influence of anesthetics on expression of c-fos mRNA was investigated. Additional animals anesthetized by isoflurane or sevoflurane were studied. Five CSDs were elicited by electric stimulation (0.5 mV, 1 second) in each animal. In situ hybridization with 35S-labeled oligonucleotides was used to evaluate the level of c-fos mRNA. The expression of c-fos was observed in the hemisphere in which CSD was elicited, but there was no difference in expression of c-fos among the groups. We conclude that volatile anesthetics can induce suppression of CSD elicitation in a dose dependent manner, but that at high concentrations sevoflurane is significantly less effective than other volatile agents. Pentobarbital has the least effect on KCl-induced CSD. These data suggest that the choice of anesthetics can impact the results of studies examining membrane depolarization and the ionic changes initiated by CSD.

No postoperative paraplegia occurred in a patient whose leg myogenic motor evoked potentials (mMEPs) disappeared during thoracoabdominal aortic aneurysm repair. A 69-year-old man underwent resection and repair of a type III (Crawford classification) thoracoabdominal aneurysm. An epidural catheter was placed into the epidural space for epidural cooling, and a Swan-Ganz catheter was placed into the subarachnoid space for cerebrospinal fluid (CSF) drainage. Continuous CSF pressure and temperature measurement was carried out the day before surgery. The mMEPs gradually disappeared 10 min after proximal double aortic clamping and complete aortic transection. Selective perfusion of intercostal arteries was started about 20 min after the loss of the mMEPs, but the mMEPs were not restored. Possibly, spinal cord hyperemia, induced by selective perfusion of the intercostal vessels, narrowed the subarachnoid space so that CSF could not be satisfactorily drained during surgery. The spinal cord hyperemia may have decreased spinal function and suppressed the leg mMEPs. The persistence of the loss of mMEPs was undeniably due to the influence of the anesthetic agent or a perfusion disorder in the lower-extremity muscles. Of note, moderate spinal cord hypothermia and postoperative CSF drainage probably resulted in improved lower-limb motor function.

We retrospectively reviewed outcomes of video-assisted thoracoscopic surgery of the esophagus (VATS-E) in the left lateral position (group L, n=70) and in the prone position (group P, n=70) in our hospital. The maximum arterial carbon dioxide tension was higher and a marked reduction in percutaneous arterial oxygen saturation was more common in group P. Moreover, the induction time of anesthesia was longer in group P, in which it was more difficult to change postural position. However, the amount of bleeding, total infusion volume, intraoperative water balance, the incidence of arrhythmia, and poor surgical field visibility during thoracic manipulation were significantly lower in group P than in group L. Thus, VATS-E in the prone position provided stable hemodynamics and safe management of patients, although there remain issues to be resolved, including respiratory care and changes in postural position.

No abstract