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P B Brechtelsbauer

Publications and source records attributed to P B Brechtelsbauer.

12 recordsLinked to original sources

Trigeminal ganglion innervation of the cochlea--a retrograde transport study.

Innervation patterns of sensory nerves from the trigeminal ganglion to the cochlear blood vessels were studied using retrograde transport of wheat germ agglutinin conjugated to horseradish peroxidase. Guinea-pigs (n=7) were unilaterally implanted with an osmotic pump and a cannula for cochlear delivery of 2% or 20% wheat germ agglutinin horseradish peroxidase (Group 1), 2% wheat germ agglutinin-horseradish peroxidase followed by 100 micromol capsaicin (Group 2), or vehicle alone. Histological sections of the trigeminal ganglia, the C1 and C2 dorsal ganglia, the superior and inferior ganglia of the glossopharyngeal nerve bilaterally, the midbrain and the brainstem were obtained after 48 h of infusion. In Group 1, a large number of labeled nerve cell bodies were observed in the anteromedial portion of the trigeminal ganglion and at the origin of the ophthalmic nerve. Some labeled cells were also found on the lateral side of the ophthalmic nerve, as well as on the medial side of the maxillary nerve root. Capsaicin pretreatment significantly reduced the density of labeled neurons in the trigeminal ganglion. A few labeled neurons were also found in the trigeminal brainstem nucleus complex and in certain auditory brainstem nuclei. No wheat germ agglutinin horseradish peroxidase-positive cells were observed in the spinal C1 or C2 cervical ganglia or in the superior or inferior glossopharyngeal ganglia. In contrast, wheat germ agglutinin-horseradish peroxidase application to the middle ear resulted in labeled cells in the middle posterolateral portion of the trigeminal ganglia and in the superior ganglia of the glossopharyngeal nerve. These results provide the first direct evidence that the trigeminal ganglion sends projections to the cochlea.

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Nitric oxide mediates capsaicin-induced increase in cochlear blood flow.

Capsaicin has been previously shown to increase cochlear blood flow (CBF) in a dose-dependent manner. The aim of this study was to define the role of nitric oxide (NO) in capsaicin-induced changes in CBF. This was investigated in the anesthetized guinea pig, utilizing laser Doppler flowmetry. Application of capsaicin (64.8 and 6.48 nmol in 2 microliters of saline) to the round window membrane (RWM) caused increases in CBF (34 +/- 2.8% of baseline (BL) and 28 +/- 2.3% BL, respectively (P < 0.001)). Application of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg intravenously or topically to the RWM) reduced blood flow in the cochlea, as previously reported. After pretreatment with i.v. L-NAME, the effect of capsaicin on CBF was significantly decreased. With the dose of capsaicin at 64.8 nmol, the increase in CBF fell from 34 +/- 2.8% BL to 6.9 +/- 1.5% BL (P < 0.001), and at 6.48 nmol it fell from 28 +/- 2.3% BL to 4.8 +/- 1.6% BL (P < 0.001). RWM L-NAME application also decreased the capsaicin vasodilatation effect. A capsaicin dose of 64.8 nmol resulted in only a 10 +/- 2.5% BL increase in CBF, and with 6.48 nmol capsaicin the increase was 7.8 +/- 2.2% of BL (P < 0.001). Capsaicin-sensitive sensory neurons in other systems are generally known to release substance P (SP), which in turn elicits release of endothelium derived relaxing factor (NO). The results of this study indicate that NO is a mediator of capsaicin-sensitive sensory neuronal function in CBF regulation.

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Autoregulation of cochlear blood flow in the hydropic guinea pig.

Previous data suggest that regulation of cochlear blood flow (CBF) may be abnormal in the hydropic guinea pig. The purpose of this study was to employ the technique of anterior inferior cerebellar artery (AICA) occlusion to measure CBF autoregulation in experimental endolymphatic hydrops. This study also addresses the role of the cochlear sympathetic neural innervation and nitric oxide in CBF regulation with hydrops. In anesthetized guinea pigs, CBF was measured with a laser Doppler flowmeter probe while the AICA was intermittently occluded with a microvascular occluder. The CBF response was measured in normal, 6-week, and 12-week chronically hydropic animals. The gain factors (0 = no autoregulation, 1 = complete autoregulation) for 1-min occlusion were 0.95 +/- 0.16 (control), 0.77 +/- 0.28 (6 week, P = 0.164), and 0.67 +/- 0.25 (12 week, P = 0.037). NG-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of nitric oxide synthase, was infused intravenously to assess basal nitric oxide (an endogenous vasodilator) production in the hydropic ear. With infusion of L-NAME, CBF was reduced by 9.16 +/- 11%, 10.7 +/- 10% (P = 0.87), and 16.6 +/- 18% (P = 0.95), in the control, 6-week, and 12-week animals, respectively. In a separate group of 12-week hydropic animals, the left superior cervical ganglion (SCG) was anesthetized with lidocaine, and AICA occlusions were performed pre- and post-blockade. Prior to blocking the SCG, the gain was 0.712 +/- 0.02 and afterwards 0.708 +/- 0.051 (P = 0.93). The above results show that there was a statistically significant reduction in CBF autoregulation in the 12-week hydropic animals. There was no difference in basal nitric oxide production in normal versus hydropic animals nor was there a change in autoregulation following blockade of the SCG. These data provide clear evidence for reduced CBF autoregulation in experimental endolymphatic hydrops.

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Basal nitric oxide production in regulation of cochlear blood flow.

Nitric oxide (NO), recently identified as endothelium-derived relaxing factor, has been shown to influence both vascular and neural function. In blood vessels, NO is produced by endothelial and smooth muscle cells and may play a role in regulation of cochlear blood flow. In the central nervous system, NO functions as a neurotransmitter involved in long term potentiation. The principle hypothesis tested in this study was that basal NO production in the cochlear blood vessels contributes to regulation of CBF. Since NO is a vasodilator, diminished NO synthesis may decrease the level of CBF. Application of a competitive inhibitor of NO synthase either intravenously or to the round window membrane caused a reduction in CBF. The application to the round window membrane did not affect compound action potential thresholds. With intravenous administration, the effect on CBF was dose-related and could be reversed with the physiologic substrate, L-arginine. These data indicate that NO is produced in the cochlear blood vessels and contributes to the regulation of CBF.

Action Potentials↗

Cochlear blood flow measured by averaged laser Doppler flowmetry (ALDF).

This report describes a new approach to estimate the hydromechanical properties of a vascular system. Averaged laser Doppler flowmetry (ALDF) was developed by averaging the flux signal of a laser Doppler flowmeter (LDF) synchronized to the heart cycle. The usefulness of this method was verified by manipulation of the cochlear microvasculature. Twelve pigmented guinea pigs under pentobarbital/fentanyl anesthesia were used. The cochlea was surgically exposed and the LDF probe placed on the bony surface of the first turn to monitor cochlear blood flow (CBF). The LDF flux signal (0.2 s time constant) was sampled by an A/D board at 2 kHz for 255 ms and averaged with synchronization to the heart beat. The mean blood flow, peak to peak amplitude, and time (phase) delay of pulsatile flow were measured from the averaged signal. According to a transmission line model of the vascular system, under a given perfusion pressure, mean flow reflects resistance while amplitude and time delay of the pulsatile flow are related to the reactance component of the impedance of the vascular system. During the formation of photochemically-induced thrombosis in the cochlear microvasculature, there was a dramatic mean flux decrease (90.1 +/- 3.4% from baseline (BL), N = 6). Additionally, a time-dependent decrease in amplitude and time delay of pulsatile flow were indicated by ALDF. These results suggest a large increase in vascular resistance and significant decrease in compliance.(ABSTRACT TRUNCATED AT 250 WORDS)

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Innervation of the endolymphatic sac.

Previous studies suggest that the endolymphatic sac plays an important role in the homeostasis of endolymph. Factors that influence blood flow in the sac may affect its function. This blood flow may be influenced by autonomic innervation; however, no such innervation has been demonstrated. The purpose of this study was to demonstrate catecholaminergic and cholinergic fibers on the endolymphatic sac. Endolymphatic sacs from Hartley guinea pigs were stained either immunocytochemically for tyrosine hydroxylase to reveal catecholaminergic fibers or histochemically for acetylcholinesterase to reveal cholinergic fibers. For tyrosine hydroxylase immunostaining, the endolymphatic sacs were treated with dilute hydrogen peroxide and then incubated in the primary antiserum. The tissue was further processed by the avidin-biotin immunoperoxidase method and reacted with diaminobenzidine. For acetylcholinesterase histochemistry, the tissue was processed by a modification of the direct thiocholine method. Light microscopy of the whole-mounted endolymphatic sacs revealed tyrosine hydroxylase-positive and acetylcholinesterase-positive fibers. Some of the acetylcholinesterase-positive fibers were clearly associated with vessels. This innervation, which has not been described previously, may significantly influence blood flow and function of the endolymphatic sac.

Acetylcholinesterase↗

Cholinergic innervation of the guinea pig tympanic membrane.

While cholinergic nerve fibers of the parasympathetic system have been demonstrated in the middle ear mucosa, such innervation of the tympanic membrane has never been shown. Such fibers may prove important since the tympanic membrane may be one of the initial sites of effusion production, and since parasympathetic innervation is thought to be involved with middle ear effusion. To demonstrate cholinergic innervation, we have used modified direct thiocholine histochemical staining. Anesthetized Hartley guinea pigs were killed, and the tympanic bullae were removed intact, fixed in 4% paraformaldehyde, and then stained whole. Following staining, the tympanic membrane was dissected from each bulla and whole-mounted for light microscopy. Numerous acetylcholinesterase-positive fibers were observed on the tympanic membrane. Some fibers appeared to be vessel associated, although the majority did not. This suggests that these fibers may act on the mucosa or vasculature of the tympanic membrane and contribute to the pathogenesis of middle ear effusion.

Acetylcholinesterase↗

Inner ear damage secondary to diabetes mellitus. I. Changes in adolescent SHR/N-cp rats.

The association between diabetes mellitus and hearing impairment has been debated in many previous studies. The spontaneous hypertensive/NIH-corpulent (SHR/N-cp) rat has been shown to be a unique genetic model for non-insulin-dependent diabetes mellitus. Seventeen diabetic and 17 control young male rats were divided into groups according to diet and phenotype. The rats were fed either 54% of sucrose or 54% starch diets for 3.5 months and killed at 5 months. The cochleas were fixed, decalcified, dissected, and stained for hair cell counting. A significant loss of outer hair cells was noted in the diabetic obese (SHR/N-cp) animals when compared with the control obese (LA/N-cp) animals in every group. Although no significant difference was noted between the diabetic obese (SHR/N-cp) animals receiving the starch and sugar diets, the diabetic obese (SHR/N-cp) animals were more severely affected than the nondiabetic lean (SHR/N-cp) rats.

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Student Research Award 1990. Catecholaminergic innervation of the inner ear.

Cochlear blood flow has been shown to be controlled, in part, by the sympathetic nervous system. We have used immunocytochemical staining for tyrosine hydroxylase (TH) to further demonstrate the extent of catecholaminergic innervation of the cochlea. Deeply anesthetized Mongolian gerbils were systemically perfused with phosphate-buffered saline, followed by 4% paraformaldehyde. The cochleae were dissected out and post-fixed for 3 hours in 4% paraformaldehyde. They were then incubated in anti-TH antibody and subsequently processed using the avidin-biotin immunoperoxidase method. Microscopic examination of whole-mounted tissue revealed many immunoreactive fibers on the spiral modiolar artery. TH-positive fibers have also been found on both radiating arterioles and radial collecting venules, which has not been previously reported. With innervation of these small vessels, blood flow in the cochlea may be segmentally controlled. We also further describe the organization of TH-positive fibers in the osseous spiral lamina.

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