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Discussion Starter #1
OK, I know that cholinomimmetics and beta blockers are useful for glaucoma
But why can't we use alpha 1 blockers? They'll cause miosis and they'll be helpful right!
 

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Well the would work, its not that they wouldn't! Its a matter of they're just never gonna be the D.O.C. for glaucoma patients because a1 antagonists are designed to target the a1 receptors in the heart, why would you want to do that???
 

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Discussion Starter #3
Well the would work, its not that they wouldn't! Its a matter of they're just never gonna be the D.O.C. for glaucoma patients because a1 antagonists are designed to target the a1 receptors in the heart, why would you want to do that???
Three points regarding your answer
First, alpha one receptors are not in the heart, they are in blood vessels.
Second, didn't they use beta blockers for glaucoma, isn't that going to affect your heart!
Third, epinephrine and ephidren are used in certain cases in glaucoma so alpha one receptors are already utilized to tackle the glaucoma problem.
 

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Discussion Starter #5
Ok here's what I think the reason;

Treatment of glaucoma is either decrease AH production or increase the outflow through the canal of schlemm
Beta blocker decrease production
M3 receptor agonist increase the outflow -- parasympathetic cause ciliary muscle contraction and relaxation of suspensory ligaments and so they aid in the outflow of the aqueous. Therefore, antimuscarinic are contraindicated.
As for alpha one receptors they are not involved in the ciliary muscle at all so the use of blocker or agonist is not going to work. However, agonists may be used to cause vasoconstriction and thereby decreasing the associated inconvenient congestion seen in open angle glaucoma.

This is just my thought of it and I have no reference
 

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This has been a tough cookie to crack, I mean almost 3 years and no conclusive answer. This answer doesn't do it for me, though.
Isn't closed angle glaucoma a condition in which the iris and the lens sort of 'stick' together, blocking drainage to the anterior chamber altogether? In that case how would giving muscarinic drugs, thereby improving the outflow through the canal of schlem, which is at the angle of the anterior chamber, improve things? Secondly if the lens and the iris are stuck together, what's so wrong with giving an alpha-1 agonist? Won't it just reduce aqueous humour formation and thereby at least buy some time until definitive surgery?
The only real explanation I see is that the resultant mydriasis would, in a sense, 'crumple' up the base of the iris at the angle where the canal of Schlem is, reducing outflow further and increasing pressure in the anterior chamber as well.
…even I'm not convinced by what I just said. Anyone else wish to take a flog at a horse which just refuses to die?
:confused:
 

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Ok! I asked an eye surgeon and this is the gist of what he said - Mydriasis in all shapes and forms is contraindicated. There's two reasons - foremost, the state of maximum apposition of the lens and iris is in MID-DILATION, which will result if you dilate a constricted pupil. Secondly, overdilation will indeed cause crumpling of the iris at the angle of the anterior chamber, compromising outflow through the canal of Schlemm.;)
 
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