Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2001
Perilymphatic and endolymphatic pressure in the guinea pig after distal dissection of the endolymphatic sac.
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Warmerdam T J, Schröder F H, Wit H P, Albers F W
Аннотация
HYPOTHESIS: The study was designed to investigate whether endolymphatic pressure exceeds perilymphatic pressure in an endolymphatic hydrops model with a partially functioning endolymphatic sac.
BACKGROUND: Previous investigations of perilymphatic and endolymphatic pressure measurements during endolymphatic hydrops were done in a classic endolymphatic hydrops model, with a surgically blocked endolymphatic duct and sac. This model, in contrast to the clinical situation of Meniere's patients, totally lacks the functional contribution of the endolymphatic sac.
METHODS: In the guinea pig, a partially functioning endolymphatic sac was created via dissection of the distal portion of the sac from the sigmoid sinus. Three (n = 5) and 6 months (n = 3) later, perilymphatic and endolymphatic pressures were measured consecutively using a WPI 900A micropressure system.
RESULTS: It was observed that damage to the distal part of the endolymphatic sac caused endolymphatic hydrops in 58% of the cases. The hydrostatic pressure in hydropic ears did not differ from that of control ears. There was no pressure difference between the perilymphatic and endolymphatic compartments in ears with endolymphatic hydrops. The endocochlear potential in ears with hydrops was statistically significantly decreased (p < 0.002).
CONCLUSION: In a hydrops model developed to be more comparable to the histopathologic appearance of Meniere's disease in the inner ear, no hydrostatic pressure difference was measured between the perilymphatic and endolymphatic spaces. The only functional difference from control ears we found was a decreased endocochlear potential.
BACKGROUND: Previous investigations of perilymphatic and endolymphatic pressure measurements during endolymphatic hydrops were done in a classic endolymphatic hydrops model, with a surgically blocked endolymphatic duct and sac. This model, in contrast to the clinical situation of Meniere's patients, totally lacks the functional contribution of the endolymphatic sac.
METHODS: In the guinea pig, a partially functioning endolymphatic sac was created via dissection of the distal portion of the sac from the sigmoid sinus. Three (n = 5) and 6 months (n = 3) later, perilymphatic and endolymphatic pressures were measured consecutively using a WPI 900A micropressure system.
RESULTS: It was observed that damage to the distal part of the endolymphatic sac caused endolymphatic hydrops in 58% of the cases. The hydrostatic pressure in hydropic ears did not differ from that of control ears. There was no pressure difference between the perilymphatic and endolymphatic compartments in ears with endolymphatic hydrops. The endocochlear potential in ears with hydrops was statistically significantly decreased (p < 0.002).
CONCLUSION: In a hydrops model developed to be more comparable to the histopathologic appearance of Meniere's disease in the inner ear, no hydrostatic pressure difference was measured between the perilymphatic and endolymphatic spaces. The only functional difference from control ears we found was a decreased endocochlear potential.