The cochlear vessels and the distribution of red blood corpuscles were studied in normotensive (N) and spontaneously hypertensive (SH) rats with and without noise exposure. The evaluation was made in a double blind manner. Ten N-rats and ten SH-rats were exposed to noise for 8 weeks and terminated immediately thereafter. The noise consisted of a 2 kHz broad noise band swept from 3 kHz to 30 kHz with a resultant equivalent sound level of 100 dB (lin) 10 h. Seven of 84 vascular parameters differed statistically at the 1% level between N- and SH-rats, and 8 and 10 parameters respectively differed for N- and SH-rats as a result of noise exposure. The observations were interpreted as indicative of a precapillary sphincter constriction in the radiating arterioles of the external wall with an upstream relative stasis and a downstream relative lack of blood, both in N- and SH-rats. In the spiral lamina the observations were interpreted as signs of a decreased blood flow after noise exposure, both in the N- and SH-animals, and most marked in the SH-animals after noise.
The vascular pattern of the rat cochlea was demonstrated by the aid of Berlin Blue (Prussian Blue) contrast. The vascular anatomy is similar to other mammals. The infrequent occurrence of the vessel of the basilar membrane under the organ of Corti is interesting in respect to its presumed importance for the oxygen supply to the hair cells. In the place where the vessel of the basilar membrane usually lies when present, a large uninjected channel was often seen throughout the cochlea. In the external wall, radiating arterioles supply and collecting venules drain all capillary areas. The vascular pattern of the external wall is well maintained at the basal end but is more sparse in apical parts of the cochlea as in other mammals. The rat cochlea is somewhat more difficult to manipulate than the cochlea in other mammals due to its small size, but the dissection of different parts of the cochlea was achieved without major problems.
and long-term changes in the cochlear vasculature and long-term changes in the sensorineuroepithelium were studied in guinea pigs after they were exposed to impulse noise. Vessel histology and cochlear hair cell loss were assessed, using a surface-preparation technique, and the results showed considerable variability. Hair cell loss and radial tears in the organ of Corti were a common finding in the animals killed four weeks after impulse-noise exposure. Impulse-noise exposure resulted in few cochlear vascular changes in the acutely and chronically affected groups. Compared with the results of our previous studies using continuous-noise exposure of different characteristics and in different mammals, this impulse-noise experiment resulted in a nonsignificant damaging effect on the cochlear vasculature. (Arch Otolaryngol 1984;110:111-115) Extensive speculations have been made concerning the traumatic mechanisms of noise on the cochlea. Among different theories to explain the sensorineural hearing loss at low¬ er sound intensities (ie, 85 to 120 dB measured on the A scale [dBA]), one proposal has been that deficient function of cochlear vessels leads to sensory cell loss. The concept is that sensory cells during increased need for oxygen and energy do not receive a sufficient supply from the cochlear vessels, possibly due to a vessel con¬ striction created by the noise itself. Most experimenters agree that me¬ chanical factors are responsible for damage to the sensorineuroep¬ ithelium at high sound intensities (ie, > 120 dBA). It is assumed that impulse-noise exposure results in tears of the cochlear membranes and other kinds of mechanical damage, eg, holes in the reticular lamina. Howev¬ er, there is little information avail¬ able concerning the specific shortterm persistent effects of impulse noise on cochlear vessels. In rats, ves¬ sel constriction in response to sound bursts can occur at intensities as low as at hearing threshold.1 Such vessel constriction in the periphery (ie, cochlea) could theoretically restrict the oxygen and energy supply and induce permanent sensory cell dam¬ age on a vascular basis. After expo¬ sure to gunshots, Kellerhals2 observed the packing of RBCs in the stria vascularis of experimental guinea pigs, which was not limited to the area of greatest hair cell damage. Stria vascularis capillaries were tightly packed with an abnormal homogenous mass of RBCs, but similar packing was absent in other vessels.These changes were present imme¬ diately and up to several days after exposure. Occlusion of lumina, col¬ lapse of vessels in the external wall of the cochlea, and degeneration of capil¬ laries with intravascular strands have been demonstrated with impulsenoise exposure.3 In animals exposed to sonic booms, hemorrhages were found in the scala tympani localized to the lower middle or basal turn of the cochlea." The mechanism was sup¬ posed to be a stretching of blood ves¬ sels on the tympanic surface of the basilar membrane, and the hemor¬ rhage was interpreted as a sign of mechanical dam...
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