Background: Preconditioning the brain with relatively safe drugs seems to be a viable option to reduce ischemic brain injury. The authors and others have shown that the volatile anesthetic isoflurane can precondition the brain against ischemia. Here, the authors determine whether isoflurane preconditioning improves long-term neurologic outcome after brain ischemia.
Methods: Six-day-old rats were exposed to 1.5% isoflurane for 30 min at 24 h before the brain hypoxia-ischemia that was induced by left common carotid arterial ligation and then exposure to 8% oxygen for 2 h. The neuropathology, motor coordination, and learning and memory functions were assayed 1 month after the brain ischemia. Western analysis was performed to quantify the expression of the heat shock protein 70, Bcl-2, and survivin 24 h after isoflurane exposure.
Results: The mortality was 45% after brain hypoxia-ischemia. Isoflurane preconditioning did not affect this mortality. However, isoflurane preconditioning attenuated ischemia-induced loss of neurons and brain tissues, such as cerebral cortex and hippocampus in the survivors. Isoflurane also improved the motor coordination of rats at 1 month after ischemia. The learning and memory functions as measured by performance of Y-maze and social recognition tasks in the survivors were not affected by the brain hypoxia-ischemia or isoflurane preconditioning. The expression of Bcl-2, a well-known antiapoptotic protein, in the hippocampus is increased after isoflurane exposure. This increase was reduced by the inhibitors of inducible nitric oxide synthase. Inducible nitric oxide synthase inhibition also abolished isoflurane preconditioning-induced neuroprotection. 相似文献
Introduction Facial nerve paralysis can be a disabling condition functionally, psychologically and aesthetically. When there has been an acquired proximal injury to the facial nerve in the presence of previously functional facial musculature, such as in acoustic neuroma surgery, neurotisation of the distal facial nerve is an appropriate choice of management. The hypoglossal nerve is most commonly used. However this is not without its limitations, notably subsequent hemilingual atrophy and facial synkinesis. We present an alternative technique of facial reinnervation utilising a motor branch of the trigeminal nerve, the nerve to masseter. We believe this technique has the potential to overcome problems encountered with use of other extra‐facial nerves. Methods Three patients with acquired facial nerve palsy following tumour resection underwent transfer of the ipsilateral masseteric nerve to facial nerve. In two patients the nerve was directly coapted to the trunk of the facial nerve while the third patient had transfer to the buccal branch. Results By twelve months postoperatively all three patients demonstrated significant improvement in facial muscle tone and symmetry at rest. All patients were able to produce a symmetrical smile with minimal synkinesis. Two of the three patients also had evidence of occasional spontaneous movements. Conclusion Use of the ipsilateral motor nerve to masseter offers an alternative technique for neurotisation of the facial nerve. The advantages of this technique include ease of dissection, constant and reliable anatomy, powerful innervation of the facial muscles, minimal donor site morbidity and the potential for return of spontaneous facial movements. 相似文献