The protein concentration of the guinea pig perilymph was investigated systematically using a micro-modification of the method of Lowry et al. Perilymph of scala vestibuli and of scala tympani was obtained from living animals and immediately post mortem by various methods. In living animals it is especially difficult to obtain samples without blood contamination. Another problem in the obtaining of perilymph from living animals is the contamination of tympanic perilymph samples with cerebrospinal fluid. This contamination diminishes the protein concentration of perilymph to a high degree. When the subarachnoid space is opened suboccipitally before perilymph extraction, there is no significant difference between protein content in tympanic and vestibular perilymph. The mean protein concentration in both cochlea scales is about 150 mg/100 ml. When samples are extracted post mortem from animals perfused intra-arterially, mean values of protein are in the same range. Without perfusion of animals, the mean value of tympanic samples extracted post mortem is significantly higher. Causes of artefacts in perilymph investigations are discussed.
Glucose, pyruvate, and lactate of perilymph (PL), blood, and cerebrospinal fluid (CSF) of unexposed and sound-exposed guinea pigs under ethyl urethane anesthesia were examined with due consideration of the principal sources of error. The animals had fasted for 15--20 h before the experiment to stabilize the blood glucose level. The metabolites were determined enzymatically by means of fluorescence measurements. It was found that the glucose levels depend not only on ingestion but also on the duration of anesthesia of the animals before sampling. The mean values of the scala tympani and scala vestibuli PL and CSF did not differ significantly, being about half those of blood or plasma immediately (10--20 min) after introducing anesthesia (Table 2). This concentration difference is in disagreement with the original ultrafiltration hypothesis of PL, suggesting a blood-PL barrier for glucose. The dependence on the duration of anesthesia and on the animals' ingestion before sampling appears to be an important cause of the differences in glucose data published in literature hitherto. No influence of anesthesia on pyruvate and lactate concentrations was observed. Data obtained on unexposed control animals (Tables 3 and 4) confirmed our earlier metabolite findings (Scheibe et al. 1976, 1981). No major changes in glucose, pyruvate, and lactate concentration of PL, blood, and CSF were detectable immediately after 1 h of exposure to wide-band noise at an intensity of 120 dB SPL. The present lactate findings confirmed our earlier exposure experiments (Scheibe et al. 1976), but they did not agree with the information given by Schnieder (1974).
Lipids of various tissues of the inner ear and the perilymph of guinea pig were investigated by the thin-layer chromatographic micro-method. The obtained qualitative results are demonstrated by chromatograms and summarized in a table. Functional investigations of the lipid metabolism of the inner earcould not be performed as yet because of methodologic difficulties.
The paper deals with: 1. the protein concentration in the perilymph (PL), the serum and the cerebrospinal fluid (CSF), 2. the protein pattern in the PL and 3. histological findings in the middle and inner ear in unilaterally ear-infected guinea pigs. The studies were performed 6 h to 21 days post infectionem (Fig. 1). The pathological changes in the middle ear, which, in most cases, were limited to the infected ear, were initially evaluated under the operating microscope and divided into 4 stages. The analytical and histological results were presented as functions of these stages. As the inflammation intensity increased, the protein concentration in the PL of the infected ears increased to a level exceeding that of the normal value more than ten times (Fig. 2). However, in the serum and in the CSF this concentration remained unchanged. Likewise, no significant protein increase in the PL of the contralateral ears was detectable in most cases. As the inflammation intensity increased, the number of the precipitation lines detectable immunoelectrophoretically increased in the PL of the infected ears (Fig. 3). An increase in the alpha1- and gamma-globulins and a decrease in Albumin was found by electrophoresis on cellulose acetate strips (Tab. 3). The histological findings correlated with initially established inflammatory stages of the middle ear mucous membrane (Tab. 4). As the inflammation intensity increased, the round window, too, was changed pathologically, so that in some cases of purulent otitis media middle ear secretion could enter the cochlea. The protein increase in the PL immediately after the infection is probably due to an increase in the blood vessel permeability in the inner ear.
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