Pentobarbital may protect against neurogenic inflammation after surgery via inhibition of substance P release from peripheral nerves of rats.

The inflammatory response related to surgery is considered surgical inflammation. Most anesthetic agents directly or indirectly suppress the immune response. However, the intravenous anesthetics pentobarbital and ketamine were reported to inhibit the lipopolysaccharide-induced inflammatory response such as cytokines formation. Neurogenic inflammation is inflammation originating from the local release of inflammatory mediators, such as substance P (SP), by primary afferent neurons after noxious stimuli like surgery. Thus, in this study, we examined whether pentobarbital and ketamine suppress SP release from cultured dorsal root ganglion (DRG) neurons. DRG cells were dissected from male Wistar rats. Released SP was measured by radioimmunoassay. We demonstrated that higher concentrations of pentobarbital (100-1,000 µM) significantly inhibited capsaicin (100 nM)-induced, but not high K+ (50 mM)-induced, SP release from DRG cells, although a high concentration of ketamine (1 mM) did not. This study revealed that pentobarbital functions between the activation of vanilloid receptor subtype 1 (TRPV1) receptors, to which capsaicin selectively binds, and the opening of voltage-operated Ca2+ channels (VOCC) in the nerve endings. Therefore, the anti-inflammatory action of pentobarbital is mediated through different mechanisms than those of ketamine. Thus, the inhibitory effect of pentobarbital on SP release from peripheral terminals may protect against neurogenic inflammation after surgery.

Comparisons of electromagnetic and piezoelectric floating-mass transducers in human cadaveric temporal bones.

Electromagnetic floating-mass transducers for implantable middle-ear hearing devices (IMEHDs) afford the advantages of a simple surgical implantation procedure and easy attachment to the ossicles. However, their shortcomings include susceptibility to interference from environmental electromagnetic fields, relatively high current consumption, and a limited ability to output high-frequency vibrations. To address these limitations, a piezoelectric floating-mass transducer (PFMT) has recently been developed. This paper presents the results of a comparative study of these two types of vibration transducer developed for IMEHDs. The differential electromagnetic floating-mass transducer (DFMT) and the PFMT were implanted in two different sets of three cadaveric human temporal bones. The resulting stapes displacements were measured and compared on the basis of the ASTM standard for describing the output characteristics of IMEHDs. The experimental results show that the PFMT can produce significantly higher equivalent sound pressure levels above 3 kHz, due to the flat response of the PFMT, than can the DFMT. Thus, it is expected that the PFMT can be utilized to compensate for high-frequency sensorineural hearing loss.

Effects of ear-canal pressurization on middle-ear bone- and air-conduction responses.

In extremely loud noise environments, it is important to not only protect one's hearing against noise transmitted through the air-conduction (AC) pathway, but also through the bone-conduction (BC) pathways. Much of the energy transmitted through the BC pathways is concentrated in the mid-frequency range around 1.5-2 kHz, which is likely due to the structural resonance of the middle ear. One potential approach for mitigating this mid-frequency BC noise transmission is to introduce a positive or negative static pressure in the ear canal, which is known to reduce BC as well as AC hearing sensitivity. In the present study, middle-ear ossicular velocities at the umbo and stapes were measured using human cadaver temporal bones in response to both BC and AC excitations, while static air pressures of +/-400 mm H(2)O were applied in the ear canal. For the maximum negative pressure of -400 mm H(2)O, mean BC stapes-velocity reductions of about 5-8 dB were observed in the frequency range from 0.8 to 2.5 kHz, with a peak reduction of 8.6(+/-4.7)dB at 1.6 kHz. Finite-element analysis indicates that the peak BC-response reduction tends to be in the mid-frequency range because the middle-ear BC resonance, which is typically around 1.5-2 kHz, is suppressed by the pressure-induced stiffening of the middle-ear structure. The measured data also show that the BC responses are reduced more for negative static pressures than for positive static pressures. This may be attributable to a difference in the distribution of the stiffening among the middle-ear components depending on the polarity of the static pressure. The characteristics of the BC-response reductions are found to be largely consistent with the available psychoacoustic data, and are therefore indicative of the relative importance of the middle-ear mechanism in BC hearing.

AMPA/kainate-type glutamate receptor antagonist reduces progressive inner hair cell loss after transient cochlear ischemia.

We investigated the effect of glutamate receptor antagonists on progressive inner hair cell (IHC) loss following transient cochlear ischemia in gerbils. Transient cochlear ischemia was induced by 15-min bilateral vertebral artery occlusion. An alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate-type glutamate receptor antagonist, 6-7-dinitroquinoxaline-2,3-dione (DNQX), or an N-methyl-D-aspartate (NMDA)-type receptor antagonist, MK-801, was administered 10 min before the ischemic insult. Hearing was assessed by sequentially recording compound action potentials (CAPs) before, during, and after the ischemia. The degree of hair cell loss in the organ of Corti was evaluated in specimens stained with rhodamine-phalloidin and Hoechst 33342. On the seventh day after ischemia, the increases in the CAP threshold and the progressive IHC loss were significantly reduced in cochleae treated with DNQX, while MK-801 was ineffective. These results suggest that the AMPA receptor plays a critical role in the development of the progressive IHC loss induced by ischemia/reperfusion injury in the cochlea.