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Alteration in capillary permeability of horseradish peroxidase in the stria vascularis and movement of leaked horseradish peroxidase after administration of furosemide.

The permeability of horseradish peroxidase (HRP) from the capillaries of the stria vascularis and the movement of leaked HRP in this site were investigated over time after the administration of furosemide, a loop diuretic, for the purpose of clarifying the function of the stria vascularis. Guinea pigs were used as experimental animals. The stria vascularis became markedly edematous at 10 min after the administration of furosemide, while the vascular permeability of HRP was decreased. This edema was thought to result not from the high permeation of strial capillaries, but from the blockage of water transport into the ductus cochlearis by inhibition of the Na+/2Cl-/K+ cotransport system on the cell membrane of the marginal cells and the exudation from the intermediate cells due to change of cell membrane permeability. A large amount of the leaked HRP from the strial capillaries was taken into vacuoles of marginal cells 1 h after furosemide administration. In the present study, no leakage of HRP was observed in the ductus cochlearis. Destroyed or degenerated cells were observed in vacuoles of marginal cells 2 and 3 h after furosemide administration, suggesting that marginal cells have a phagocytic function. Two hours after furosemide administration, the vascular permeability of HRP and the function of intermediate cells was still at a decreased level, although the stria vascularis was almost restored to normal morphology. Three hours after furosemide treatment, the vascular permeability of HRP and the intake of HRP into intermediate cell vesicles were generally normalized, suggesting near restoration of stria vascularis function. In the non-furosemide-treated control group, no vacuolation was observed in marginal cells, nor was HRP intake observed in these cells.

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