2007 Volume 100 Issue 2 Pages 73-82
When the cochleas of guinea pigs were fixed after decapitation, HRP leakage from the strial capillaries was observed with blood sludge. HRP was transported to the extracapillary space by many pinocytotic vesicles and marginal folds. However, when the cochleas were fixed before decapitation, blood sludge was not observed in the strial capillaries and leakage of HRP from the capillaries was not observed 10 minutes after HRP injection. Thereafter, the level of HRP leakage increased with time. It was noted that capillary permeability to HRP at the basal turn was lower than that of the upper three turns. HRP leakage was not observed in the capillaries of the spiral ligament even beyond one hour after injection.
As a result of severe hemorrhagic shock in guinea pigs, blood sludge appeared in strial capillaries and capillary permeability to HRP increased. However, in moderate hemorrhagic shock, both blood sludge and accentuation of capillary permeability did not occur.
After the inoculation of endotoxin in the middle ear, a large amount of HRP leaked out of the capillaries through the opened endothelial cell junctions.
After vibration administered to auditory ossicle is by a drill, the permeability of the strial capillaries to HRP also increased. High permeability was thought to be caused by damage to the strial endothelial cells. HRP leakage initially took place through the tubules in the endothelial cytoplasm, and HRP leaked in to the extracapillary space when the cell membranes were damaged by vibration. Administration of the steroid inhibited HRP leakage from the strial capillaries.
The stria vascularis became markedly edematous after the administration of furosemide, while capillary permeability to HRP was decreased.
From the above, the route of HRP leakage is different depending on the type of stimulation, even if it occurs alongside increased capillary permeability.