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Outflow Resistance (outflow + resistance)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Dexamethasone alters F-actin architecture and promotes cross-linked actin network formation in human trabecular meshwork tissue

CYTOSKELETON, Issue 2 2005
Abbot F. Clark
Abstract Elevated intraocular pressure is an important risk factor for the development of glaucoma, a leading cause of irreversible blindness. This ocular hypertension is due to increased hydrodynamic resistance to the drainage of aqueous humor through specialized outflow tissues, including the trabecular meshwork (TM) and the endothelial lining of Schlemm's canal. We know that glucocorticoid therapy can cause increased outflow resistance and glaucoma in susceptible individuals, that the cytoskeleton helps regulate aqueous outflow resistance, and that glucocorticoid treatment alters the actin cytoskeleton of cultured TM cells. Our purpose was to characterize the actin cytoskeleton of cells in outflow pathway tissues in situ, to characterize changes in the cytoskeleton due to dexamethasone treatment in situ, and to compare these with changes observed in cell culture. Human ocular anterior segments were perfused with or without 10,7 M dexamethasone, and F-actin architecture was investigated by confocal laser scanning microscopy. We found that outflow pathway cells contained stress fibers, peripheral actin staining, and occasional actin "tangles." Dexamethasone treatment caused elevated IOP in several eyes and increased overall actin staining, with more actin tangles and the formation of cross-linked actin networks (CLANs). The actin architecture in TM tissues was remarkably similar to that seen in cultured TM cells. Although CLANs have been reported previously in cultured cells, this is the first report of CLANs in tissue. These cytoskeletal changes may be associated with increased aqueous humor outflow resistance after ocular glucocorticoid treatment. Cell Motil. Cytoskeleton 60:83,95, 2005. © 2004 Wiley-Liss, Inc. [source]

The effect of scleral flap edge apposition on intraocular pressure control in experimental trabeculectomy

CLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 4 2008
Wayne Birchall
Abstract Background:, To assess the contribution of scleral flap edge apposition to intraocular pressure (IOP) control in trabeculectomy, using a previously described and validated experimental model of guarded filtration surgery. Materials and methods:, Twelve rectangular-flap trabeculectomy operations each with two apical adjustable sutures were performed on six donor human eyes connected to a constant flow infusion with real-time IOP monitoring. Three sizes of scleral flap were created: 4 × 4 mm, 16 mm2 (n = 4), 3 × 3 mm, 9 mm2 (n = 4) or 3 × 2 mm, 6 mm2 (n = 4). Sutures were tied tightly to produce high aqueous outflow resistance, and equilibrium IOP established. The lateral and posterior edges of the scleral flap were removed, the sutures tightened again, and the new equilibrium IOP measured. Results:, Following flap closure and with intact flap edges, the mean absolute IOP for all flaps (n = 12) was 19.5 ± 3.9 mm Hg (mean ± SD, range 12.4,27 mm Hg) and following flap edge excision 18.7 ± 4.4 mm Hg (range 5.6,27.9 mm Hg), demonstrating no significant difference between flaps with edge apposition compared with those without (P = 0.33). Mean relative IOP (% of baseline) was 68.4 ± 12.1% (range 40.9,94%) with intact flap edges and 65.4 ± 14.5% (range 18.5,97.2%) following flap edge excision (P = 0.31). Flaps measuring 4 × 4 mm and 3 × 3 mm behaved in a similar manner with minimal change in equilibrium IOP following excision of flap edges. Conclusions:, In this experimental model, scleral flap edge apposition is not required for generating outflow resistance. Suture tension generated during tight flap closure produces apposition of the underside of the scleral trapdoor to the underlying bed, and it is this apposition, which determines IOP. [source]

Regional Variations of Contractile Activity in Isolated Rat Lymphatics

MICROCIRCULATION, Issue 6 2004
ANATOLIY A. GASHEV
ABSTRACT Objective: To evaluate lymphatic contractile activity in different regions of the lymphatic system in a single animal model (the rat thoracic duct, mesenteric, cervical, and femoral lymphatics) in response to changes in lymph pressure and flow. Methods: The systolic and diastolic diameters of isolated, cannulated, and pressurized lymphatic vessels were measured. Contraction frequency, ejection fraction, and fractional pump flow were determined. The influences of incrementally increased transmural pressure (from 1 to 9 cm H2O) and imposed flow (from 1 to 5 cm H2O transaxial pressure gradient) were investigated. Results: The authors determined regional differences in lymphatic contractility in response to pressure and imposed flow. They found the highest pumping (at the optimal pressure levels) in mesenteric lymphatics and lowest pumping in thoracic duct. All lymphatics had their optimal pumping conditions at low levels of transmural pressure. Different degrees of the flow-induced inhibition of the pump were observed in the different types of lymphatics. During high flow, the active lymph pumps in thoracic duct and cervical lymphatics were almost completely abolished, whereas mesenteric and femoral lymphatics still exhibited significant active pumping. Conclusions: The active lymph pumps in different regions of the rat body express variable relative strengths and sensitivities that are predetermined by different hydrodynamic factors and regional outflow resistances in their respective locations. [source]