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Canal of Schlemm

FIGURE 24-1. In the normal eye, aqueous humor flows through the ciliary body into the posterior chamber, through the pupil into the anterior chamber, and out through the trabecular meshwork to the canal of Schlemm into the venous drculation. [Pg.222]

The fluid escapes into the canal of Schlemm at a rate of about 6 ml./day.1... [Pg.53]

The principal determinants of lOP are the rate of aqueous fluid production by the ciliary epithelium and the rate of fluid drainage (outflow) in the canal of Schlemm. Aqueous fluid production involves passive, near-isosmolar fluid secretion driven by active salt transport across the ciliary epithelium. Ion and solute transporters have been identified on pigmented and non-pigmented layers of the ciliary epithelium that probably facilitate active solute secretion. Aqueous fluid drainage is believed to involve pressure-driven bulk fluid flow in the canal of Schlemm, as well as fluid movement through the sclera by seepage across the ciliary muscle and supraciliary space. [Pg.45]

Structures of the anterior chamber of the eye. Tissues with significant autonomic functions and the associated ANS receptors are shown in this schematic diagram. Aqueous humor is secreted by the epithelium of the ciliary body, flows into the space in front of the iris, flows through the trabecular meshwork, and exits via the canal of Schlemm arrow). Blockade of the 13 adrenoceptors associated with the ciliary epithelium causes decreased secretion of aqueous. Blood vessels (not shown) in the sclera are also under autonomic control and influence aqueous drainage. [Pg.126]

Muscarinic agonists instilled into the conjunctival sac cause contraction of the smooth muscle of the iris sphincter (resulting in miosis) and of the ciliary muscle (resulting in accommodation). As a result, the iris is pulled away from the angle of the anterior chamber, and the trabecular meshwork at the base of the ciliary muscle is opened. Both effects facilitate aqueous humor outflow into the canal of Schlemm, which drains the anterior chamber. [Pg.137]

Acute angle closure glaucoma has been reported as rare complication of rapid insulin therapy for hyperglycemic non-ketotic coma (20). It was postulated that raised glucose concentrations in the lens leads to increased sorbitol and water influx. The osmotic changes in the lens are not immediately corrected when the glucose concentration in aqueous humor is lowered, and this can lead to obstruction of the canal of Schlemm and increased intraocular pressure. [Pg.393]

Muscarinic cholinomimetics mediate contraction of the circular pupillary constrictor muscle and of the ciliary muscle. Contraction of the pupillary constrictor muscle causes miosis, a reduction in pupil size. Miosis is usually present in patients exposed to large systemic or small topical doses of cholinomimetics, especially organophosphate cholinesterase inhibitors. Ciliary muscle contraction causes accommodation of focus for near vision. Marked contraction of the ciliary muscle, which often occurs with cholinesterase inhibitor intoxication, is called cyclospasm. Ciliary muscle contraction also puts tension on the trabecular meshwork, opening its pores and facilitating outflow of the aqueous humor into the canal of Schlemm. Increased outflow reduces intraocular pressure, a very useful result in patients with glaucoma. All of these effects are prevented or reversed by muscarinic blocking drugs such as atropine. [Pg.126]

Reversible cholinesterase inhibitors find their greatest clinical use in the treatment of open-angle glaucoma. Relief is achieved by enhancing the contraction of the ciliary muscle and the iris sphincter. This contracture pulls the iris off the lens and facilitates fluid movement through the canal of Schlemm. The result is decreased pressure with reduced distortion of the lens and increased movement of aqueous humor out of the anterior chamber of the eye. [Pg.210]

The ciliary epithelium in the posterior chamber secretes aqueous humour. The aqueous humour flows in between the cornea and iris. After filtration through the trabecular meshwork, it returns to the venous circulation via the canal of Schlemm. [Pg.290]

Q8 Normal IOP is 15 mmHg (range is 10-20 mmHg). It is maintained by a balance between the secretion of aqueous humour by the ciliary body and its flow into the canal of Schlemm via the trabecular meshwork. Glaucoma is present when IOP rises to >21 mmHg. [Pg.291]

The uveal vessels remove drugs by bulk transport from the iris and ciliary body.The direct outflow pathway from aqueous humor through trabecular meshwork and canal of Schlemm into the episcleral vessels is another major source of drug removal from the eye. [Pg.25]

Expected Gonioscopic Findings. From anterior to posterior, the following structures are present in the angle Schwalbe s line (representing the posterior border of Descemet s membrane), the anterior trabecular mesh-woik (often less pigmented than the posterior trabecular meshwork), the canal of Schlemm within the botmdaries of and deep to the trabecular meshwork (typically only visible if filled with venous blood), the posterior trabecular meshwork, the scleral spur (to which the ciliary muscle is attached), and the ciliary body band. [Pg.675]

Pilocarpine is direct acting cholinergic used to treat glaucoma, reducing intraocular pressure by constricting pupils and opening the canal of Schlemm, which enable drainage of aqueous humor. [Pg.213]

Reduction of intraocular pressure in some types of glaucoma, by increasing the drainage of intraocular fluid through the canal of Schlemm. [Pg.40]

An acute (painful) or chronic (genetic) condition with increased IOP due to blockade of the canal of Schlemm. Emergency drug management prior to surgery usually involves cholinomimetics, carbonic anhydrase inhibitors, and/or mannitol. [Pg.63]

Carbachol, pilocarpine, echothiophate Cholinomimetic Activation of M receptors causes contraction of ciliary muscle, which increases flow through the canal of Schlemm echothiophate is an organophosphate AChE inhibitor - T outflow... [Pg.64]

Answer C. This question helps review ANS drug actions on the eye. The pupil is controlled reciprocally by the SANS (iris dilator, alpha) and the PANS (iris sphincter, muscarinic) thus, alpha agonists cause mydriasis, and AChE inhibitors cause miosis (answers D and E are opposites ). Ciliary muscle contraction is controlled by the PANS, so choli-nomimetics lower IOP by putting tension on the trabecular network to facilitate outflow of aqueous humor through the canal of Schlemm—beta blockers decrease the secretory activity of ciliary epithelial cells (answers A and B are opposites ). Topical use of nonse-lective beta blockers can indeed worsen asthma ... [Pg.80]

Latanoprost PGF2(X analog T Outflow through canal of Schlemm... [Pg.357]

This drug is commonly used in the therapy of glaucoma. It produces miosis and contraction of the ciliary muscle, which allows drainage from the canals of Schlemm, decreasing intraocular... [Pg.88]

Timolol is a nonselective (5-receptor antagonist that is used topically in the therapy of glaucoma. The antagonism of (5 receptors on the radial muscle of the iris results in miosis, which facilitates drainage of humor into the canals of Schlemm. Timolol is also used in the therapy of angina and vasospastic infarct. [Pg.103]


See other pages where Canal of Schlemm is mentioned: [Pg.214]    [Pg.222]    [Pg.422]    [Pg.422]    [Pg.429]    [Pg.188]    [Pg.197]    [Pg.124]    [Pg.179]    [Pg.188]    [Pg.157]    [Pg.126]    [Pg.481]    [Pg.482]    [Pg.551]    [Pg.346]    [Pg.23]    [Pg.179]    [Pg.188]    [Pg.107]    [Pg.117]    [Pg.63]    [Pg.87]    [Pg.372]    [Pg.1099]    [Pg.1099]   
See also in sourсe #XX -- [ Pg.87 ]




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