High frequency jet ventilation at the distal end of tracheostenosis during flexible bronchoscopic resection of large intratracheal tumor: Case series.

INTRODUCTION: Resection of a large intratracheal tumor with severe obstruction via flexible bronchoscope remains a formidable challenge to anesthesiologists. Many artificial airways positioned proximal to tracheal obstruction can not ensure adequate oxygen supply. How to ensure effective gas exchange is crucial to the anesthetic management. PATIENT CONCERNS: Five patients of intratracheal tumor occupying 70% to 85% of the tracheal lumen were scheduled for tumor resection via flexible bronchoscope. DIAGNOSIS: The patients were diagnosed with intratracheal tumor based on their symptoms, radiographic findings and tracheoscopy. INTERVENTIONS: We describe a technique of high frequency jet ventilation (HFJV) using an endobronchial suction catheter distal to tracheostenosis during the surgery, which ensured the good supply of oxygen. We applied general anesthesia with preserved spontaneous breathing. A comprehensive anesthesia protocol that emphasizes bilateral superior laryngeal nerve (SLN) block and sufficient topical anesthesia. An endobronchial suction catheter was introduced transnasally into the trachea and then advanced through the tracheostenosis with the tip proximal to the carina under direct vision with the aid of fiber bronchoscope. HFJV was then performed through the suction catheter. OUTCOMES: The SPO2 maintained above 97% during the surgery. Carbon dioxide retention was alleviated obviously when adequate patency of the trachea lumen achieved about 30 min after the beginning of surgery. HFJV was ceased and all patients had satisfactory spontaneous breathing at the end of the procedure. CONCLUSION: HFJV at the distal end of tracheostenosis is a suitable ventilation strategy during flexible bronchoscopic resection of a large intratracheal tumor.

Isoflurane protects against injury caused by deprivation of oxygen and glucose in microglia through regulation of the Toll-like receptor 4 pathway.

Oxygen and glucose deprivation (OGD) are the most important factors related to tissue damage resulting from stroke. Microglial cells have been found to be very vulnerable to ischemia and OGD. It has been reported that isoflurane exposure can protect the mammalian brain from insults such as ischemic stroke; however, the effects of isoflurane on OGD-induced injury in microglia are as yet unknown. In this study, we investigated the effects of isoflurane on OGD-induced injury in microglia. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and lactate dehydrogenase (LDH) revealed that OGD did indeed induce cell death in microglia. However, isoflurane preconditioning attenuated OGD-induced cell death. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay demonstrated that isoflurane treatment alleviated OGD-induced apoptosis. Toll-like receptor 4 (TLR4) plays a considerable role in the induction of innate immune and inflammatory responses. Our results indicate that isoflurane preconditioning inhibits the upregulation of TLR4 as well as the activation of its downstream molecules, such as c-Jun N-terminal kinase (JNK) and nuclear factor kappa B (NF-κB), in BV-2 microglia exposed to OGD. Importantly, we also found that isoflurane pretreatment significantly reduces the production of proinflammatory factors such as tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), IL-ß, and nitric oxide (NO). The results indicate that TLR4 and its downstream NF-κB-dependent signaling pathway contribute to the neuroprotection of microglia exposed to OGD/reoxygenation by administration of isoflurane.