[Characteristics of blood-optic nerve barrier: experiment with rats].

OBJECTIVE: To investigate the difference of endothelial cells in ultrastructure, marker expression, and permeability between blood-brain barrier and blood-optic nerve barrier. METHODS: The optic nerve, including the prelaminar region, lamina cribrosa, retro-laminar region, intraorbital portion, intracanalicular portion, and intracranial portion, and frontal cortex of 20 male SD rats were obtained to undergo electron microscopy and immunohistochemistry was used to detect the expression of endothelial barrier antigen (EBA) and the extravasation of fibrinogen around the microvessels. RESULTS: Electron microscopy showed tight junction among the endothelial cells in the microvessels of all portions of optic nerve and cerebral cortex. The number of plasmalemmal vesicles of the prelaminar region was (108.0 +/- 12.0)/microm2, significantly greater than that of the cerebral cortex [(31.8 +/- 2.9)/microm2, P < 0.05]. However, there was no significantly difference in the number of plasmalemmal vesicle among the other portion of optic nerve and cerebral cortex (all P > 0.05). Immunohistochemistry showed that EBA was negative in the endothelial cells in the microvessels of prelaminar region, but strongly positive in the microvessels in the other portions of the optic nerve and in the cerebral cortex. Fibrinogen was present around the microvessels in the prelaminar region of optic nerve in a small amount, however, not present in the other portions of optic nerve and cerebral cortex. CONCLUSION: There is significant differences in the number of plasmalemmal vesicle, EBA expression, and permeability between the prelaminar region of optic nerve and cerebral cortex, which demonstrates that this region lacks the characteristics of typical blood-brain barrier. However, the other parts of optic nerve possess the properties of classical blood-brain barrier.

TRPV4 channels in the human urogenital tract play a role in cell junction formation and epithelial barrier.

AIM: The molecular interactions between transient receptor potential vanilloid subtype 4 channels (TRPV4) and cell junction formation were investigated in the human and mouse urogenital tract. MATERIALS AND METHODS: A qualitative study was performed to investigate TRPV4 channels, adherence junctions (AJs) and tight junctions (TJs) in kidney, ureter and bladder tissues from humans and wild-type and transgenic TRPV4 knockout (-/-) mice with immunohistochemistry, Western blotting, immunoprecipitation and reverse trasnscription-PCR. Cell junction formation in the wild-type and TRPV4 knockout (-/-) mouse was evaluated with immunohistochemistry and transmission electron microscope (TEM) techniques. RESULTS: TRPV4 channels are predominantly located in membranes of epithelial cells of the bladder, ureter and the collecting ducts of the kidney. There is a molecular interaction between the TRPV4 channel and the AJ. TEM evaluation showed that AJ formation is disrupted in the TRPV4 -/- mouse resulting in deficient intercellular connections and integrity of the epithelium. CONCLUSIONS: TRPV4 is believed to be a mechanoreceptor in the bladder. This study demonstrates that TRPV4 is also involved in intercellular connectivity and structural integrity of the epithelium.

Effects of arterial ischemia and venous congestion on the lumbar nerve root in dogs.

The development of radiculopathy in patients with lumbar canal stenosis is thought to be closely related to intraradicular edema resulting from compression. However, there is little agreement as to question which is more essential for intermittent claudication: ischemia or congestion. The aim of the present experimental investigation was to examine the effect of ischemia and congestion on the nerve root using dogs. The aorta was clamped as an ischemia model of the nerve root and the inferior vena cava was clamped as a congestion model at the sixth costal level for 30 min using forceps transpleurally. Measurements of blood flow, partial oxygen pressure, and conduction velocity in the nerve root were repeated over a period of 1 h after release of clamping. Finally, we examined the status of intraradicular blood-nerve barrier under fluorescence and transmission electron microscope. Immediately after clamping of the inferior vena cava, the central venous pressure increased by about four times and marked extravasation of protein tracers was induced in the lumbar nerve root. Blood flow, partial oxygen pressure, and conduction velocity of the nerve root were more severely affected by aorta clamp, but this ischemia model did not show any intraradicular edema. The blood-nerve barrier in the nerve root was more easily broken by venous congestion than by arterial ishemia. In conclusion, venous congestion may be an essential factor precipitating circulatory disturbance in compressed nerve roots and inducing neurogenic intermittent claudication.