Glaucoma

Glaucoma

      

• K
  Strenn, B Matulla, M Wolzt, et al (Univ of Vienna)
  
  
  Reversal of
  Endothelin-1-induced Ocular Hemodynamic Effects by
  Low-dose Nifedipine in Humans.  
  Clin
  Pharmacol Ther 63:54-63, 1998
  
    
  
  Calcium
  channel blockers may be beneficial in patients with
  normal-tension glaucoma and vasospastic reactions. 
  Calcium channel blockers (CCB) may increase
  ocular-blood flow and have a functional antagonism
  with endothelin-1 (ET-1) in the ocular vasculature.
  
    
  
  Nifedipine
  reverses ET-1 induced constriction in ocular
  vasculature at doses that do not affect systemic
  hemodynamics.  This
  suggests some association between the therapeutic
  effect of CCBs and the endothelin system in patients
  with normal tension glaucoma.
  
   
  
  The
  above findings provide a rationale for studying
  low-dose nifedipine as a supplementary medication in
  patients with glaucoma.
  
    

• thoe
  Schwartzenberg GWS, Trope GE (Univ of Toronto)
  
  Anorexia, Depression and Dementia induced
  by Dorzolamide Eyedrops (Trusopt)
  
  Can
  J Ophthalmol 34: 93-94, 1999
  
    
  
  This
  is a case report of a patient with systemic adverse
  effects of topical dorzolamide.
  
    
  
  The
  case report highlights the importance of the
  awareness of side effects of all topical medications
  used for glaucoma.
  
     
  

• Lill-Inger Larsson, (Uppsala Univ. Hospital, Uppsala, Sweden)
  
  Aqueous Humor Flow in Normal Human Eyes Treated with Brimonidine and Timolol, Alone and in Combination.
  
  Arch Ophthalmol, April 2001; vol.119, pg.492-495
  
    
  
  Topically applied 2% brimonidine tartrate was compared with topical 0.5% timolol maleate alone, and in combination, in a randomized, double-masked, placebo-controlled study of 20 human subjects.
  
     
  
  Brimonidine reduced aqueous humor flow by 33.1%, timolol by 49.9%, and the combination of brimonidine and timolol by 58.9%. Brimonidine reduced the IOP by 20.3%, timolol by 22.9%, and the combination by 34.7%.
  
    
  
  The results of this study indicate that brimonidine suppresses aqueous humor formation, but not as efficiently as timolol.
  
     
  
  When timolol and brimonidine were applied in combination a further reduction of aqueous humor flow and IOP was seen.
  
    
  
  Evidence supports the theory that brimonidine has some additional ocular hypotensive effect through enhancement of aqueous outflow.
  
       
  

• Tian
  B, Geiger B, Epstein DL, et al (Univ of Wisconsin,
  Madison; Weizmann Inst of Sciences, Rehovot, Israel;
  Duke Univ, Durham, NC)
  
  Cytoskeletal Involvement in the Regulation of
  Aqueous Humor Ouflow.
  
  Invest Ophthalmol Vis Sci 41: 619-623, 2000.
  
      
  
  Fluid flow in the anterior chamber supplies oxygen
  and nutrients to the nonvascularized cornea, lens
  and the trabecular meshwork.
  
    
  
  Potential long-term therapeutic benefits for
  lowering intraocular pressure (IOP) are offered by
  compounds with cytoskeletal effects.
  
     
  
  The usual IOP reducing agents either suppress
  production of aqueous humor or increase outflow
  through ciliary muscle, consequently reducing
  aqueous flow through a compromised trabecular
  meshwork and posing a threat to the cornea and lens.
  
    
  
  Recent studies reveal that the cytoskeleton of the
  trabecular meshwork {TM} may be involved in
  regulation of aqueous humor outflow.
  
    
  
  A cytoskeletal agent acting directly on the TM/Schlemm’s
  canal to reduce outflow resistance may be more
  consistent with normal physiologic function.
  
    
  
  Arrays of collagen beams covered by endothelium like
  cells form the TM.
  
   
  
  The cytoskeleton consists of a complex system of
  cytoplasmic fibers which form a number of cellular
  processes.
  
    
  
  The different filament networks are microfilaments,
  microtubules and intermediate filaments.
  Cytochalasins disrupt the actin cytoskeleton
  
   
  
  Ethacrynic acid works by inhibiting microtubule
  assembly IN VITRO.
  
     
  
  H-7 inhibits actino-myosin-driven contractility and
  induces general cellular relaxation.
  
    
  
  Lantruculins alter cell shape and disrupt
  microfilament organization. Staurosporine
  chelerythrine, ML-7, and the protein kinase
  C-activator phorbol ester have been shown to
  decrease outflow resistance in monkeys.
  
    
  
  Further research on the biomolecular differences
  between the cornea and TM may facilitate the
  development of TM – selective drugs that could
  reduce outflow resistance without affecting other
  eye tissues.