Red blood cell (RBC) surface acetylcholinesterase showing a hemorheological pattern during glaucoma treatment

Clin Hemorheol Microcirc. 2006;35(1-2):149-54.

Abstract

Background: Glaucoma is currently attributed to two different possible pathogenetic mechanisms: mechanical (the ocular damage is induced by physical injury), and vascular (the ocular damage is sustained by ischemia of the optic nerve head).

Aim: We considered the possibility that several anti-glaucoma drugs (beta-blockers, carbonic anhydrase inhibitors and prostaglandins) could have an influence on optic nerve head hemorheology and oxygen supply.

Materials and method: We studied 4 groups of 10 subjects each: a control group, and 3 primary open angle glaucoma (POAG) groups, treated with topical beta-blockers, (10 patients), carbonic anhydrase inhibitors (CAI), and prostaglandin analogs (PG), respectively. In these 4 groups we investigated the RBC surface AchE and cytosolic calcium levels in order to assess their possible influence on the hemorheology and microcirculation in optic nerve head blood perfusion.

Results: A significant correlation (p < 0.048) was found between the RBC surface acetylcholinesterase and RBC intracytosolic calcium values in patients with POAG treated with beta-blockers. We found no significant correlation (p = n.s.) between the same patterns in the other Groups or in Controls.

Conclusion: These data indicate that CAI and PG drugs do not interfere with AchE in POAG patients, whereas beta-blockers negatively affect the RBC deformability.

Publication types

  • Clinical Trial

MeSH terms

  • Acetylcholinesterase / drug effects*
  • Adrenergic beta-Antagonists / pharmacology
  • Calcium / blood*
  • Carbonic Anhydrase Inhibitors / pharmacology
  • Erythrocytes / drug effects
  • Erythrocytes / enzymology*
  • Erythrocytes / physiology
  • Female
  • Glaucoma, Open-Angle / blood
  • Glaucoma, Open-Angle / drug therapy*
  • Glaucoma, Open-Angle / enzymology
  • Hemorheology
  • Humans
  • Linear Models
  • Male
  • Middle Aged
  • Prostaglandins, Synthetic / pharmacology

Substances

  • Adrenergic beta-Antagonists
  • Carbonic Anhydrase Inhibitors
  • Prostaglandins, Synthetic
  • Acetylcholinesterase
  • Calcium