The demonstration of nitric oxide in cochlear blood vessels in vivo and in vitro: the role of endothelial nitric oxide in venular permeability.

The objectives of the current study were to investigate the distribution and production of NO in cochlear blood vessels, and to assess whether the inhibition of basal NO production leads to vascular protein leakage of the cochlear microvasculature. Using the fluorescent dye 4,5-diaminofluorescein diacetate, NO was detected, both in vitro and in vivo, in the endothelial cells of various cochlear blood vessels, including the spiral modiolar artery, the vessel of the basilar membrane and the vessels of the spiral osseous lamina. Vessel leakage was assessed using intravital fluorescence microscopy following systemic infusion of fluorescein isothiocyanate-labeled bovine albumin. Local perfusion of the cochlear basal turn with either Ringer's solution or Ringer's containing an inactive nitric oxide synthase inhibitor (100 microM) produced minimal protein leakage. Perfusion with the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (100 microM) produced significantly enhanced vascular protein leakage. The findings demonstrate the presence of endothelial NO in the cochlear blood vessels and suggest that NO protects cochlear venules against excessive vascular leakage.