Background The role of the cerebral venous system （CVS） in intracranial pressure （ICP） regulation remains largely unclear. In the present study, the interaction between ICP and the cerebral venous system and its p...Background The role of the cerebral venous system （CVS） in intracranial pressure （ICP） regulation remains largely unclear. In the present study, the interaction between ICP and the cerebral venous system and its possible mechanism were investigated with respect to the biological characteristics of the cerebral venous system and its hemodynamic response under increased ICP. Methods We created intracranial hypertension animal model, measured and calculated the venous flow velocity and diameter of the outflow terminal of the CVS with color ultrasonic system and recorded the vascular morphology by 3-dimensional anatomical microscopy. Patients who suffered from raised ICP underwent MRI and digital subtraction angiography （DSA） examination to show the length in the vertical direction of the wall of the bridging vein representing the diameter value. Pathological autopsy was performed from bodies of patients who had died from non-cerebral causes to observe the juncture part between the venous sinuses and tributary vertical brain veins. Results Under increased ICP conditions, venous drainage through the outlet cuff segment, a unique structure between the bridge vein and sinus, was obstructed and in turn venous blood became congested. Therefore, the increased blood volume worsened the pre-existing ICP according to the well-accepted theory regarding volume-pressure relationship. This phenomenon was described as concurrent ＇k, enogenic intracranial hypertension＂, which is characterized by intracranial venous blood stasis responsive to and together with the original increased ICP. Conclusions The existence of this special pathophysiological process is prevalent, rather than rare, in various intracraniAI disorders. Thi.~ findinn would definitAIv nrovide new insinht into the. Area of cerebral venous svstem research.展开更多
Background Elevated intraocular pressure （lOP） is primarily due to increased aqueous outflow resistance, but how aqueous outflow resistance is generated and regulated are still not fully understood. The aim of this ...Background Elevated intraocular pressure （lOP） is primarily due to increased aqueous outflow resistance, but how aqueous outflow resistance is generated and regulated are still not fully understood. The aim of this study is to determine whether changes in outflow facility, outflow pattern, and morphology following acute lOP elevation were reversible when the lOP was returned to a normal level in bovine eyes using a two-color tracer technique to label outflow patterns within the same eye. Methods Twelve fresh enucleated bovine eyes were perfused with Dulbecco＇s phosphate buffer saline （PBS） containing 5.5 mmol/L glucose （DBG） at 30 mmHg first to establish the baseline outflow facility followed by a fixed volume of red fluorescent microspheres （0.5 μm, 0.002% v/v）. After the red tracer being replaced with DBG in the anterior chamber, perfusion was continued at 7 mmHg with the same volume of green tracer, followed by a fixative. In two control groups, the eyes were constantly perfused at either 30 mmHg （n=6） or 7 mmHg （n=6） using the same methods. The outflow facility （C, pJ.min.-lmmHg-1）, was continuously recorded. Confocal images were taken along the inner wall （IW） of the aqueous plexus （AP） in frontal sections. The percent of the effective filtration length （PEFL, PEFL=IW length exhibiting tracer labeling/total length of IW） was measured. Sections with AP were processed and examined by light microscopy. The total length of IW and the length exhibiting separation （SL） in the juxtacanalicular connective tissue （JCT） were measured. A minimum of eight collector channel （CC） ostia per eye were analyzed for herniations. Results In the experimental （30-7 mmHg） group, the outflow facility was significantly higher at 7 mmHg （（4.81±1.33） #lmin-1 mmHg-1） than that at 30 mmHg （（0.99±0.15） μl.min-1 mmHg-1, P=-0.002）, corresponding to a significant increase in the PEFL （P=-0.0003）. The percent of CC ostia exhibiting herniations in the experimental group （（67.40±8.90） μl.min·-1mmHg-1） decreased significantly compared to that in the control at 30 mmHg （（94.44±3.33） μl.min-lmmHg-1, P=-0.03）, but higher than that in the control at 7 mmHg （（29.43±4.60） μl.min-1mmHg-1, P=0.01）. Washout-associated separation between the IW and JCT was found by light microscopy and percent separation length （PSL, PSL=SL/total length of IW） was decreased in the control at 30 mmHg compared to that in the experimental group and control at 7 mmHg. Conclusions The pressure-induced morphological and hydrodynamic changes were reversible. Changes （collapse of AP, separation between the JCT and IW, and herniation into CC ostia） influence the effective filtration area that regulates outflow facility.展开更多
文摘Background The role of the cerebral venous system （CVS） in intracranial pressure （ICP） regulation remains largely unclear. In the present study, the interaction between ICP and the cerebral venous system and its possible mechanism were investigated with respect to the biological characteristics of the cerebral venous system and its hemodynamic response under increased ICP. Methods We created intracranial hypertension animal model, measured and calculated the venous flow velocity and diameter of the outflow terminal of the CVS with color ultrasonic system and recorded the vascular morphology by 3-dimensional anatomical microscopy. Patients who suffered from raised ICP underwent MRI and digital subtraction angiography （DSA） examination to show the length in the vertical direction of the wall of the bridging vein representing the diameter value. Pathological autopsy was performed from bodies of patients who had died from non-cerebral causes to observe the juncture part between the venous sinuses and tributary vertical brain veins. Results Under increased ICP conditions, venous drainage through the outlet cuff segment, a unique structure between the bridge vein and sinus, was obstructed and in turn venous blood became congested. Therefore, the increased blood volume worsened the pre-existing ICP according to the well-accepted theory regarding volume-pressure relationship. This phenomenon was described as concurrent ＇k, enogenic intracranial hypertension＂, which is characterized by intracranial venous blood stasis responsive to and together with the original increased ICP. Conclusions The existence of this special pathophysiological process is prevalent, rather than rare, in various intracraniAI disorders. Thi.~ findinn would definitAIv nrovide new insinht into the. Area of cerebral venous svstem research.
文摘Background Elevated intraocular pressure （lOP） is primarily due to increased aqueous outflow resistance, but how aqueous outflow resistance is generated and regulated are still not fully understood. The aim of this study is to determine whether changes in outflow facility, outflow pattern, and morphology following acute lOP elevation were reversible when the lOP was returned to a normal level in bovine eyes using a two-color tracer technique to label outflow patterns within the same eye. Methods Twelve fresh enucleated bovine eyes were perfused with Dulbecco＇s phosphate buffer saline （PBS） containing 5.5 mmol/L glucose （DBG） at 30 mmHg first to establish the baseline outflow facility followed by a fixed volume of red fluorescent microspheres （0.5 μm, 0.002% v/v）. After the red tracer being replaced with DBG in the anterior chamber, perfusion was continued at 7 mmHg with the same volume of green tracer, followed by a fixative. In two control groups, the eyes were constantly perfused at either 30 mmHg （n=6） or 7 mmHg （n=6） using the same methods. The outflow facility （C, pJ.min.-lmmHg-1）, was continuously recorded. Confocal images were taken along the inner wall （IW） of the aqueous plexus （AP） in frontal sections. The percent of the effective filtration length （PEFL, PEFL=IW length exhibiting tracer labeling/total length of IW） was measured. Sections with AP were processed and examined by light microscopy. The total length of IW and the length exhibiting separation （SL） in the juxtacanalicular connective tissue （JCT） were measured. A minimum of eight collector channel （CC） ostia per eye were analyzed for herniations. Results In the experimental （30-7 mmHg） group, the outflow facility was significantly higher at 7 mmHg （（4.81±1.33） #lmin-1 mmHg-1） than that at 30 mmHg （（0.99±0.15） μl.min-1 mmHg-1, P=-0.002）, corresponding to a significant increase in the PEFL （P=-0.0003）. The percent of CC ostia exhibiting herniations in the experimental group （（67.40±8.90） μl.min·-1mmHg-1） decreased significantly compared to that in the control at 30 mmHg （（94.44±3.33） μl.min-lmmHg-1, P=-0.03）, but higher than that in the control at 7 mmHg （（29.43±4.60） μl.min-1mmHg-1, P=0.01）. Washout-associated separation between the IW and JCT was found by light microscopy and percent separation length （PSL, PSL=SL/total length of IW） was decreased in the control at 30 mmHg compared to that in the experimental group and control at 7 mmHg. Conclusions The pressure-induced morphological and hydrodynamic changes were reversible. Changes （collapse of AP, separation between the JCT and IW, and herniation into CC ostia） influence the effective filtration area that regulates outflow facility.
