Biomedical subjects

N K Woolf

Publications and source records attributed to N K Woolf.

40 records · Page 3Linked to original sources

PubMedDate not supplied

Cochlear pathophysiology associated with inner ear immune responses.

The effects of primary and secondary inner ear immune responses were investigated in the guinea pig. Subjects were immunized with keyhole limpet hemocyanin (KLH). Serum and perilymph anti-KLH titers, cochlear microphonic (CM) and VIII nerve N1 compound action potential (AP) thresholds, and cochlear morphology were examined at 2 or 4 weeks post-inner ear KLH inoculation. Primary inner ear immunized subjects developed serum and perilymph anti-KLH titers, exhibited minimal cochlear histopathology and showed only small changes in CM and AP thresholds at 2 or 4 weeks post-inner ear inoculation. Secondary immune response animals, those which were systemically immunized with KLH prior to inner ear challenge, showed significant serum and perilymph anti-KLH titers, and normal CM and AP thresholds at the time of inner ear challenge. At 2 or 4 weeks following inner ear challenge, secondary immunized animals showed very significant increases in CM and AP thresholds, and marked cochlear histopathology. We conclude that secondary inner ear challenge results in significant cochlear pathophysiology, while primary inner ear immunization does not.

Action Potentials↗

PubMedDate not supplied

Changes in cochlear blood flow during acoustic stimulation as determined by 14C-iodoantipyrine autoradiography.

Local blood flow was measured in the tissues of the cochlea using the [14C]iodoantipyrine autoradiographic technique. Flow observed without acoustic stimulation was compared with that seen during exposure to wide-band noise at 85 or 105 dB SPL. Compared with the unexposed cochlea, substantial increases in blood flow were observed during exposure to 85 dB SPL noise in the spiral ganglion, VIII nerve and spiral lamina. Little or no change was noted in external wall structures. These results are consistent with changes in cochlear metabolism which have been reported previously using similar techniques, suggesting that increases in blood flow may be linked to increases in local metabolism. No changes in blood flow were measured during exposure to 105 dB SPL noise. This result is similar to those of other investigators using potentially damaging intensities of acoustic stimulation.

Acoustic Stimulation↗

PubMedDate not supplied

Temporal sequence of viral antigen expression in the cochlea induced by cytomegalovirus.

Injection of guinea-pig cytomegalovirus into seronegative guinea pig cochleas results in viral labyrinthitis. The location of infected cells 1-8 days following inoculation was examined using an immunohistochemical assay for viral antigens. Mesothelial cells below the basilar membrane and those lining the scala tympani, especially below the osseous spiral lamina, were the first cells to express antigen. This occurred 2 days following inoculation. Infection then spread rapidly toward the brain and through the perilymphatic duct to involve inflammatory cells, mesothelial cells of Reissner's membrane, spiral ganglion cells, and the vestibular ganglion cells. In any one cochlea, more mesothelial cells and inflammatory cells expressed viral antigen than any other cell type. It seems then, that there is a differential susceptibility to viral infection and antigen expression in the various cell types of the cochlea. Typical cytomegalic inclusions were common in mesothelial cells. However, many cells labelled for viral antigens did not contain inclusions. The identification of viral antigens then, is a more sensitive technique for demonstrating infection than is the location of cytomegalic inclusion cells.

Animals↗

PubMedDate not supplied

Hearing loss in experimental cytomegalovirus infection of the guinea pig inner ear: prevention by systemic immunity.

Guinea pig cytomegalovirus (GPCMV) has been used to establish a reproducible model of viral labyrinthitis and hearing loss. Cochlear function was assessed by electrophysiological recordings of cochlear microphonic (CM) and eighth nerve N1 compound action potential (AP) thresholds prior to and up to eight days following inoculation of the scala tympani. Inner ear inoculation of seronegative subjects with live GPCMV produced profound elevations in CM and AP thresholds: 70% of these subjects had their thresholds raised to the limits of the sound system throughout the tested frequency range of 0.10 to 32 kHz. Histopathologic effects associated with CM and AP threshold shifts were primarily limited to the perilabyrinthine compartment, and were greatest in the most basal cochlear turns. Systemic infection with GPCMV produced an immune response, but did not affect CM or AP thresholds. Subsequent inoculation of the inner ear of these seropositive animals with live GPCMV did not result in either CM or AP threshold shifts, or cochlear histopathology. Inoculations of inactivated virus into the inner ears of seronegative and seropositive animals produced only moderate CM and AP threshold effects. Primary GPCMV labyrinthitis thus results in significant cochlear dysfunction and histopathologic changes which are prevented by prior systemic infection with GPCMV.

Animals↗