Perivascular delivery of neomycin inhibits the activation of NF-kappaB and MAPK pathways, and prevents neointimal hyperplasia and stenosis after arterial injury.

The nuclear transcription factor kappaB (NF-kappaB) is a cytoplasmic dimer that, as the family of mitogen-activated protein kinase (MAPK), can directly regulate the expression of early genes and genes involved in the stress response, following a variety of physiological or pathological stimuli. Both of them stimulate the transcription of many proteins, which are considered important during inflammation. A crucial role has been assigned to these factors in cellular proliferation and in neointimal hyperplasia secondary to the endothelial lesion of arterial vessels. On the other hand, it has been described that neomycin can have an inhibitory function on tumor cell proliferation, through the inhibition of different intracellular pathways of signaling, among them the NF-kappaB and MAPK pathways. Rat common carotid artery was subjected to balloon angioplasty. Neomycin sulfate (18 mg) was applied using pluronic acid gel on the adventitial surface of the injured vessel. MAPK and NF-kappaB activation was quantified after 24 hours with immunohistochemical staining. Neointimal formation was quantified after 14 days with morphometry. Immunohistochemistry results demonstrating MAPK and NF-kappaB activation reveal that both transcription factors are activated in the media of the control vessel wall. In contrast, the immunoreactivity for MAPK and NF-kappaB in the sections obtained from arteries treated with neomycin over 24 hours was insufficient or nonexistent. Treatment with neomycin on adventitia over 14 days in arteries on which angioplasty was performed shows a neointimal index (intimal area/medial area) decrease of 71% in comparison with arteries that were not treated. The adventitial neomycin treatment over 14 days produces a very significant increase (287.5%; p<0.0001) in the arterial luminal circumference in comparison with arteries treated with vehicle. These results support the theory that neomycin plays an important role against neointimal hyperplasia through the inhibition of MAPK and NF-kappaB activation.

Usefulness of monitoring brain tissue oxygen pressure during awake craniotomy for tumor resection: a case report.

Awake craniotomy is indicated for surgical resection of tumors located near eloquent areas of the brain. The anesthetic technique is based on a combination of local anesthesia, sedation, and analgesia. Usually only clinical parameters are assessed and no other cerebral oxygenation monitoring techniques are applied. The authors report the use of brain tissue oxygen pressure monitoring during awake craniotomy. A 48-year-old right-handed man with a left temporoparietal mass was scheduled for awake craniotomy, cortical stimulation, and selective tumor removal. Monitoring included electrocardiography, pulse oximetry, end-tidal CO2, bladder temperature, invasive and noninvasive arterial pressure, and brain tissue oxygen pressure (PtiO2). The anesthetic technique consisted of continuous perfusions of 0.02 to 0.05 microg/kg/min remifentanil, propofol (target concentration, 0.5 to 1.2 microg/mL), and 25 to 50 microg/kg/min esmolol, and local anesthetic blockade of the head pin insertion sites and surgical incision area (a mixture of 0.2% ropivacaine, 1% lidocaine, and epinephrine, 1:200 000). Intraoperative cortical stimulation was performed to guide the resection according to the patient's verbal response. A change in PtiO2 was observed, gradually falling from 28 mm Hg at the beginning of the intervention down to 3 mm Hg. At this stage, surgical resection was concluded. On arrival at the intensive care unit, mixed dysphasia and slight weakness of the right arm were noted. Three weeks after surgery, the patient's speech is improving and the motor deficit has disappeared. This case suggests a possible role of PtiO2 in awake craniotomy as an aid in detecting intraoperative adverse events, but further experience with PtiO2 in this setting is needed.