Pharmacological protection of reoxygenation damage to in vitro brain slice tissue.

Pharmacological protection of central neural function against damage by hypoxia and reoxygenation was studied electrophysiologically and biochemically in hippocampal brain slices. Hypoxia causes a loss of both orthodromically and antidromically evoked potentials in CA1 pyramidal cell neurons. Damage due to hypoxia lasting more than 10 min cannot be restored by reoxygenation. Following pretreatment with methylprednisolone (10(-5) M), indomethacin (10(-5) M) or allopurinol (10(-5) M), reoxygenation after 10 min of hypoxia resulted in complete recovery of the evoked activity. Na+,K+-ATPase activity was not reduced by 10 min of hypoxia, but was reduced by 50% during the first 10 min of subsequent reoxygenation. Allopurinol (10(-5) M) protected against loss of this enzyme activity. The protective action by these drugs of both electrophysiological and biochemical aspects of neural function is consistent with the hypothesis that secondary ischemic damage is caused by the formation of oxygen-derived free radicals during reperfusion.

Characterization of the immune barrier in human olfactory mucosa.

Immunologic defense factors in the human olfactory mucosa were localized immunohistochemically. Olfactory epithelium was identified with an antiserum to olfactory marker protein, specific for olfactory receptor neurons. Constituents of the secretory immune system, including IgA, IgM, secretory component, and J chain, were localized in the acinar and duct cells of Bowman's glands and in the mucociliary complex. In addition, B lymphocytes in the lamina propria near Bowman's glands displayed immunoreactivity for IgA, IgM, and J chain. Immunostaining also localized other humoral factors. Immunoreactivity for IgG was present throughout the stroma and in B lymphocytes in the lamina propria. Antibody to IgD stained numerous B lymphocytes clustered below the basement membrane. Antibody to IgE stained similarly distributed cells; toluidine blue staining demonstrated that many were mast cells. In addition, antibodies to IgD and IgE stained occasional intraepithelial B lymphocytes or mast cells. Two antimicrobial proteins, lactoferrin and lysozyme, were localized in Bowman's glands and the mucociliary complex. Thus, the human olfactory mucosa, which provides a direct neural route for pathogens to the brain, is a site for synthesis and secretion of immune and other defense factors.

Use of dilute epinephrine as an aid in facial nerve monitoring.

Facial nerve monitoring during otologic and neurotologic procedures has been previously described, and its use is becoming routine. Although these procedures are done under general anesthesia, lidocaine is often used as a vehicle for epinephrine to aid hemostasis during the procedure. The routine use of lidocaine in these preparations presents the theoretical and sometimes real problem of anesthetizing the facial nerve at the start of the procedure, thereby invalidating subsequent attempts at monitoring and stimulation. We present the data from our experience with 74 patients using an epinephrine solution 1:100,000 for infiltration without any local anesthetic. We have found this procedure to be effective in maintaining hemostasis, quite safe and well tolerated, and without adverse effects on the desired monitoring of the facial nerve.