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The effect has been studied of intravenously administered glycerol on paracellular and cellular transport of macromolecular HRP tracer in the lateral cochlear wall. The findings indicate osmotically induced diffusion phenomena by the opening of shunt pathways through junctional complexes in the stria vascularis. Vesicular transport is accelerated, direction of transport however is not affected by the changed osmolality.

Ferritin transport through the strial capillary during kanamycin intoxication was examined under a transmission electron microscope. Twelve guinea pigs were treated intramuscularly with kanamycin (400 mg/kg/day) for 2-3 weeks. When full hearing loss was recognized by estimating the Preyer reflex or auditory brain-stem response (ABR), ferritin was given intravenously and animals were sacrificed 1/3, 1, and 2 h later. At 1/3 h, ferritin was present diffusely not only in the endothelial cell but also in the basal lamina and within vesicles in the strial cell. Alternatively, it was discharged into the endolymphatic space. At 2 h, ferritin was seen on the luminal surface and in the cytoplasm of the endolymphatic cells of Reissner's membrane. These results suggest that the basal lamina of the strial capillary was altered qualitatively by kanamycin administration.

We tested the hypothesis that furosemide interferes with energy generation in the cochlea, and determined its effect on CO2 formation from glucose and glyceroaldehyde-3-phosphate dehydrogenase (GAPDH) activity by examining biochemical and histochemical changes in the cochlea, the kidney, and the liver. We found that furosemide suppressed CO2 formation in vitro at relatively low concentrations in all tissues examined. GAPDH was inhibited as soon as 2 min after its administration (80 mg/kg, i.v.). Recovery of this enzyme activity was most rapid in the liver. We concluded that furosemide does interfere with energy generation in the cochlea, kidney, and liver as a result of its inhibition of GAPDH.

The microscopical and ultramicroscopical changes in the stria vascularis due to cis-diamminedichloroplatinum II (DDP) were studied. Sixteen healthy adult guinea pigs were used for the experiment. A standard dosage DDP (1.5 mg/kg/d) was administered over a period of 5-20 days. A clear degeneration pattern was found (ranging from no changes to cystic degeneration with protrusion of marginal cells followed by loss of marginal cells). DDP seems to be especially toxic for marginal cells in stria vascularis in the guinea pig.

Following several studies on the effects of kanamycin toxicity on the inner ears of guinea pigs, we have studied the importance of melanin in this phenomenon. Transmission electron microscopy showed that, under the influence of kanamycin, the intermediate strial cells developed a secretory aspect similar to that seen in skin melanocytes. This aspect as yet has never been described for the inner ear cells. A planimetric, morphometric method was also used to determine the strial cell melanin status in control animals. Additional findings in the study confirmed an increase in the number of melanosomes during kanamycin poisoning. Statistical data are discussed.

A freeze-fracture examination of the stria vascularis during the first 2 h after injection of ethacrynic acid was performed. This showed a re-distribution of the particles on the membrane fracture faces of both marginal and intermediate cells. As oedematous spaces developed, particle-poor, vesicle-like structures were found associated with both cell types. The tight junctions at the apices of the marginal cells and around basal cells were unaffected.

Using the microprobe for energy dispersive X-ray microanalysis, the elemental compositions of both the individual cells of the stria vascularis and of the endolymph were followed simultaneously under normal conditions and after the administration of 120 mg/kg ethacrynic acid (EA). Marginal cells and intermediate cells showed reversible increases in potassium and decreases in sodium concentrations. Shifts in the ionic composition of endolymph occurred later than after elemental changes in the strial cells. The present results indicate that the marginal and the intermediate cells are the primary target for EA-induced ototoxicity. However, generalized toxic effects of EA are also indicated, with a general leakage of different elements occurring during the 30-60 min period after EA administration.

Ultrastructural changes in the guinea pig spiral prominence were studied at various times after a single intravenous injection of ethacrynic acid (40 mg/kg body-weight). Initial swelling of endolymph-facing epithelial cells was followed by dilatation of the intercellular spaces and marked shrinkage of the stroma cells surrounding the spiral prominence vessel. While the changes in the stria vascularis and the spiral prominence progressed at about the same pace, the regression to normal ultrastructure set in earlier in the spiral prominence.