scholarly journals Acoustic Trauma Modulates Cochlear Blood Flow and Vasoactive Factors in a Rodent Model of Noise-Induced Hearing Loss

2019 ◽  
Vol 20 (21) ◽  
pp. 5316 ◽  
Author(s):  
Sun-Ae Shin ◽  
Ah-Ra Lyu ◽  
Seong-Hun Jeong ◽  
Tae Hwan Kim ◽  
Min Jung Park ◽  
...  

Noise exposure affects the organ of Corti and the lateral wall of the cochlea, including the stria vascularis and spiral ligament. Although the inner ear vasculature and spiral ligament fibrocytes in the lateral wall consist of a significant proportion of cells in the cochlea, relatively little is known regarding their functional significance. In this study, 6-week-old male C57BL/6 mice were exposed to noise trauma to induce transient hearing threshold shift (TTS) or permanent hearing threshold shift (PTS). Compared to mice with TTS, mice with PTS exhibited lower cochlear blood flow and lower vessel diameter in the stria vascularis, accompanied by reduced expression levels of genes involved in vasodilation and increased expression levels of genes related to vasoconstriction. Ultrastructural analyses by transmission electron microscopy revealed that the stria vascularis and spiral ligament fibrocytes were more damaged by PTS than by TTS. Moreover, mice with PTS expressed significantly higher levels of proinflammatory cytokines in the cochlea (e.g., IL-1β, IL-6, and TNF-α). Overall, our findings suggest that cochlear microcirculation and lateral wall pathologies are differentially modulated by the severity of acoustic trauma and are associated with changes in vasoactive factors and inflammatory responses in the cochlea.

2007 ◽  
Vol 121 (8) ◽  
pp. 721-724 ◽  
Author(s):  
D-Y Xu ◽  
Y-D Tang ◽  
S-X Liu ◽  
J Liu

AbstractEndothelin 1 is a vasoconstrictive peptide with many biological functions. To investigate the distribution of endothelin 1 in guinea pig cochlear lateral wall and the significance of endothelin 1 in maintaining cochlear homeostasis, the immunohistochemistry avidin biotin complex method was applied by using rabbit anti-endothelin 1 polyclonal antibody as primary antibody. Endothelin-1-like activities were detected in the marginal cells, spiral prominence epithelial cells, outer sulcus cells, stria vascularis capillaries, basal cells and spiral ligament fibrocytes.These results suggest that endothelin 1 may play an important role in maintaining cochlear homeostasis.


2009 ◽  
Vol 267 (2) ◽  
pp. 205-205
Author(s):  
Martin Canis ◽  
Warangkana Arpornchayanon ◽  
Catalina Messmer ◽  
Markus Suckfuell ◽  
Bernhard Olzowy ◽  
...  

2003 ◽  
Vol 51 (7) ◽  
pp. 903-912 ◽  
Author(s):  
Toshihiro Suzuki ◽  
Tetsuro Takamatsu ◽  
Masahito Oyamada

To elucidate whether the two different gap junction proteins connexin43 (Cx43) and connexin26 (Cx26) are expressed and localized in a similar manner in the adult rat cochlea, we performed three-dimensional confocal microscopy using cryosections and surface preparations. In the cochlear lateral wall, Cx43-positive spots were localized mainly in the stria vascularis and only a few spots were present in the spiral ligament, whereas Cx26-positive spots were detected in both the stria vascularis and the spiral ligament. In the spiral limbus, Cx43 was widely distributed, whereas Cx26 was more concentrated on the side facing the scala vestibuli and in the basal portion. In the organ of Corti, Cx43-positive spots were present between the supporting cells but they were fewer and much smaller than those of Cx26. These data demonstrated distinct differences between Cx43 and Cx26 in expression and localization in the cochlea. In addition, the area of overlap of zonula occludens-1 (ZO-1) immunolabeling with Cx43-positive spots was small, whereas it was fairly large with Cx26-positive spots in the cochlear lateral wall, suggesting that the differences are not associated with the structural difference between carboxyl terminals, i.e., those of Cx43 possess sequences for binding to ZO-1, whereas those of Cx26 lack these binding sequences.


1992 ◽  
Vol 101 (4) ◽  
pp. 355-359 ◽  
Author(s):  
Kensuke Watanabe ◽  
Atsushi Komatsuzaki

Membranous cytoplasmic bodies (MCBs) were observed both in the intermediate cells of the stria vascularis and in the fibrocytes of the spiral ligament in normal cats. The MCBs in the intermediate cells were round or ovoid, ranged from 1 to 5 μm in diameter, and consisted of 2 to 40 or more layers disposed concentrically about a core. The core was composed of not only cytoplasm but also of mitochondria in various stages of disintegration, empty vacuoles, and many kinds of dense bodies similar to lysosomes. The MCBs in the fibrocytes were similar to those in the intermediate cells, but they were a little smaller in diameter and consisted of fewer than 10 layers. Both in the intermediate cells and in the fibrocytes, MCBs seem to have a phagocytic function.


1998 ◽  
Vol 118 (5) ◽  
pp. 576-583 ◽  
Author(s):  
Benzion Goldwyn ◽  
Mumtaz J. Khan ◽  
Bhagyalakshmi G. Shivapuja ◽  
Michael D. Seidman ◽  
Wayne S. Quirk

The cause of noise-induced hearing loss remains unclear despite years of both epidemiologic and experimental investigation. Among the many possible pathophysiologic mechanisms that may contribute to noise-induced temporary or permanent threshold shifts are insufficiencies in cochlear blood flow. Although the literature is inconsistent, several histologic and physiologic studies demonstrate signs of reduced circulation in the cochlea after noise exposure. Recent studies using computer-enhanced intravital microscopy complement these earlier findings. Evidence suggests that these microcirculatory events are mediated in part by several circulating factors, including the potent vasoactive peptide angiotensin. This study investigated this possibility by pretreating with the angiotensin receptor antagonist sarthran during noise exposure and examining both cochlear microcirculation and auditory sensitivity. The results of these experiments show noise-induced ischemia in the lateral wall of the cochlea and temporary threshold shifts. Treatment with sarthran prevented this noise-induced microcirculatory ischemia and preserved auditory sensitivity at the low frequencies tested. These findings support a role for the angiotensinergic system during noise exposure and suggest that preservation of cochlear blood flow is functionally related to auditory sensitivity. (Otolaryngol Head Neck Surg 1998;118:576–83.)


2006 ◽  
Vol 291 (5) ◽  
pp. C1038-C1048 ◽  
Author(s):  
Toshiaki Shibata ◽  
Hiroshi Hibino ◽  
Katsumi Doi ◽  
Toshihiro Suzuki ◽  
Yasuo Hisa ◽  
...  

Cochlear endolymph has a highly positive potential of approximately +80 mV known as the endocochlear potential (EP). The EP is essential for hearing and is maintained by K+ circulation from perilymph to endolymph through the cochlear lateral wall. Various K+ transport apparatuses such as the Na+,K+-ATPase, the Na+-K+-2Cl− cotransporter, and the K+ channels Kir4.1 and KCNQ1/KCNE1 are expressed in the lateral wall and are known to play indispensable roles in cochlear K+ circulation. The gastric type of the H+,K+-ATPase was also shown to be expressed in the cochlear lateral wall (Lecain E, Robert JC, Thomas A, and Tran Ba Huy P. Hear Res 149: 147–154, 2000), but its functional role has not been well studied. In this study we examined the precise localization of H+,K+-ATPase in the cochlea and its involvement in formation of EP. RT-PCR analysis showed that the cochlea expressed mRNAs of gastric α1-, but not colonic α2-, and β-subunits of H+,K+-ATPase. Immunolabeling of an antibody specific to the α1 subunit was detected in type II, IV, and V fibrocytes distributed in the spiral ligament of the lateral wall and in the spiral limbus. Strong immunoreactivity was also found in the stria vascularis. Immunoelectron microscopic examination exhibited that the H+,K+-ATPase was localized exclusively at the basolateral site of strial marginal cells. Application of Sch-28080, a specific inhibitor of gastric H+,K+-ATPase, to the spiral ligament as well as to the stria vascularis caused prominent reduction of EP. These results may imply that the H+,K+-ATPase in the cochlear lateral wall is crucial for K+ circulation and thus plays a critical role in generation of EP.


2011 ◽  
Vol 301 (1) ◽  
pp. H69-H78 ◽  
Author(s):  
T. Wu ◽  
M. Dai ◽  
X. R. Shi ◽  
Z. G. Jiang ◽  
A. L. Nuttall

The cochlear lateral wall generates the endocochlear potential (EP), which creates a driving force for the hair cell transduction current and is essential for normal hearing. Blood flow at the cochlear lateral wall is critically important for maintaining the EP. The vulnerability of the EP to hypoxia suggests that the blood flow in the cochlear lateral wall is dynamically and precisely regulated to meet the changing metabolic needs of the cochlear lateral wall. It has been reported that ATP, an important extracellular signaling molecule, plays an essential role in regulating cochlear blood flow. However, the cellular mechanism underlying ATP-induced regional blood flow changes has not been investigated. In the current study, we demonstrate that 1) the P2X4 receptor is expressed in endothelial cells (ECs) of spiral ligament (SL) capillaries. 2) ATP elicits a characteristic current through P2X4 on ECs in a dose-dependent manner (EC50 = 0.16 mM). The ATP current has a reversal potential at ∼0 mV; is inhibited by 5-(3-bromophenyl)-1,3-dihydro-2 H-benzofuro[3,2- e]-1,4-diazepin-2-one (5-BDBD), LaCl3, pyridoxal phosphate-6-azo(benzene-2,4-disulfonic acid) tetrasodium salt hydrate (PPADS), and extracellular acidosis; and is less sensitive to α,β-methyleneadenosine 5′-triphosphate (α,β-MeATP) and 2′- and 3′- O-(4-benzoyl-benzoyl) adenosine 5′-triphosphate (BzATP). 3) ATP elicits a transient increase of intracellular Ca2+ in ECs. 4) In accordance with the above in vitro findings, perilymphatic ATP (1 mM) caused dilation in SL capillaries in vivo by 11.5%. Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME), a nonselective inhibitor of nitric oxide synthase, or 5-BDBD, the specific P2X4 inhibitor, significantly blocked the dilation. These findings support our hypothesis that extracellular ATP regulates cochlear lateral blood flow through P2X4 activation in ECs.


1989 ◽  
Vol 101 (3) ◽  
pp. 375-384 ◽  
Author(s):  
M. J. LaRouere ◽  
J. S. Sillman ◽  
A. L. Nuttall ◽  
J. M. Miller

Many inner ear disorders may be caused by alterations in cochlear blood flow (CBF). However, each measurement technique used to monitor CBF has limitations in examining the relationship between otopathologic states and blood flow. This study Investigates laser Doppler flowmetry (LDF) and its fundamental drawback: The unknown relationship of LDF output to actual CBF. LDF readings are directly compared with concurrent intravital microscopy (IVM) measures of erythrocyte velocity in the lateral wall of the guinea pig cochlea. Positive end expiratory pressure, spontaneous respiration of 5% and 10% carbon dioxide, phenylephrine, and direct electrical stimulation of the cochlea were used to manipulate CBF. High, positive correlations were found between simultaneous LDF and IVM measurements of CBF. In addition, the study demonstrated that current microdissection techniques used to perform IVM do not cause changes in CBF. IVM measurements of CBF are a more sensitive indicator of CBF changes than are LDF measures. Despite the high correlation between measurement techniques within a single manipulation, simultaneous LDF and IVM measurements differed between manipulations. This may reflect regional changes in CBF affected by these manipulations and differences in the sampled vascular beds contributing to these two measures. It is unlikely that a single calibration factor can be defined that would allow the conversion of LDF output to actual units of blood flow across different manipulations used to alter CBF.


1981 ◽  
Vol 90 (3) ◽  
pp. 264-266 ◽  
Author(s):  
Tsutomu Nakashima ◽  
Akikazu Ito

A study was done to determine how increased fluid pressure in the inner ear influences cochlear blood flow. Hydrostatic pressure was applied to the scala vestibuli or scala tympani in guinea pigs. Endocochlear potential, which is sensitive to the lack of oxygen, was measured through the round window membrane or through the stria vascularis. Cochlear blood flow was confirmed by intravenous injection of India ink. When the perilymphatic pressure was raised to a relatively high level, endocochlear potential decreased, in a similar way as in response to anoxia, because of the cessation of the cochlear blood flow. This change was completely reversible upon applications of pressure for brief periods of time. We consider that the cochlear blood flow ceases when the fluid pressure reaches the level of intracochlear arterial pressure.


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