J Korean Ophthalmol Soc.  2011 Sep;52(9):1089-1093.

Effects of Pupil Dilation and Constriction Agents on Trabecular Meshwork Cells

Affiliations
  • 1Department of Ophthalmology, Catholic University of Daegu College of Medicine, Daegu, Korea. jwkim@cu.ac.kr

Abstract

PURPOSE
To investigate the effects of pupil dilation and constriction agents on the survival and production of nitric oxide (NO) in cultured human trabecular meshwork cells (HTMC).
METHODS
Primarily cultured HTMC were exposed to 0, 0.01, and 0.1 mg/ml of tropicamide, cyclopentolate, atropine, or pilocarpine for 2 hours. Cellular survival and production of NO were assessed using the MTT assay and Griess assay, respectively.
RESULTS
Tropicamide, cyclopentolate, atropine, and pilocarpine decreased cellular survival at the concentration of 0.1 mg. At the concentration of 0.01 mg/ml, all agents decreased production of NO to some extent, although the reduction was not statistically significant.
CONCLUSIONS
Pupil dilation and constriction agents may be toxic to HTMC if used at high concentrations or if used frequently in the short-term but may not affect trabecular outflow.

Keyword

Atropine; Cyclopentolate; Pilocarpine; Trabecular meshwork cells; Tropicamide

MeSH Terms

Atropine
Constriction
Cyclopentolate
Humans
Nitric Oxide
Pilocarpine
Pupil
Trabecular Meshwork
Tropicamide
Atropine
Cyclopentolate
Nitric Oxide
Pilocarpine
Tropicamide

Figure

  • Figure 1. Effects of tropicamide on the survival of trabecular meshwork cells. Tropicamide decreased cellular survival. * p < 0.05.

  • Figure 2. Effects of cyclopentolate on the survival of trabecular meshwork cells. Cyclopentolate decreased cellular survival. * p < 0.05.

  • Figure 3. Effects of atropine on the survival of trabecular meshwork cells. Atropine decreased cellular survival. * p < 0.05.

  • Figure 4. Effects of pilocarpine on the survival of trabecular meshwork cells. Pilocarpine decreased cellular survival. * p < 0.05.

  • Figure 5. Effects of 0.01 mg/ml tropicamide, cyclopentolate, atropine, and pilocarpine on the production of nitric oxide in trabecular meshwork cells. All agents did not affect the production of nitric oxide significantly compared to the non-exposed control. p > 0.05.


Reference

References

1. Abraham SV. Mydriatic glaucoma: a statistical study. Arch Ophthalmol. 1933; 10:757–62.
2. Nelson ME, Orton HP. Counteracting the effects of mydriatics: Does it benefit the patient? Arch Ophthalmol. 1987; 105:486–9.
3. Siam GA, de Barros DS, Gheith ME, et al. The amount of intraocular pressure rise during pharmacological pupillary dilatation is an indicator of the likelihood of future progression of glaucoma. Br J Ophthalmol. 2007; 91:1170–2.
Article
4. Wiederholt M. Direct involvement of trabecular meshwork in the regulation of aqueous humor outflow. Curr Opin Ophthalmol. 1998; 9:46–9.
Article
5. Moncada S, Palmer RM, Higgs EA. Nitric oxide: physiology, pathophysiology, and pharmacology. Pharmacol Rev. 1991; 43:109–42.
6. Bredt DS, Snyder SH. Nitric oxide: a physiologic messenger molecule. Annu Rev Biochem. 1994; 63:175–95.
Article
7. Brüne B, Knethen A, Sandau KB. Nitric oxide and its role in apoptosis. Eur J Pharmacol. 1998; 351:261–72.
Article
8. Nathanson JA, McKee M. Identification of an extensive system of nitric oxide-producing cells in the ciliary muscle and outflow pathway of the human eye. Invest Ophthalmol Vis Sci. 1995; 36:1765–73.
9. Geyer O, Podos SM, Mittag T. Nitric oxide synthase activity in tissues of the bovine eye. Graefes Arch Clin Exp Ophthalmol. 1997; 235:786–93.
Article
10. Meyer P, Champion C, Schlotzer-Schrehardt U, et al. Localization of nitric oxide synthase isoforms in porcine ocular tissues. Curr Eye Res. 1999; 18:375–80.
Article
11. Schuman JS, Erickson K, Nathanson JA. Nitrovasodilator effects on intraocular pressure and outflow facility in monkeys. Exp Eye Res. 1994; 58:99–105.
Article
12. Wang RF, Podos SM. Effect of the topical application of nitro-glycerin on intraocular pressure in normal and glaucomatous monkeys. Exp Eye Res. 1995; 60:337–9.
Article
13. Nathanson JA, McKee M. Alterations of ocular nitric oxide synthase in human glaucoma. Invest Ophthalmol Vis Sci. 1995; 36:1774–84.
14. Matsuo T. Basic nitric oxide production is enhanced by hydraulic pressure in cultured human trabecular cells. Br J Ophthalmol. 2000; 84:631–5.
15. Schneemann A, Dijkstra BG, van den Berg TJ, et al. Nitric ox-ide/guanylate cyclase pathways and flow in anterior segment perfusion. Graefes Arch Clin Exp Ophthalmol. 2002; 240:936–41.
Article
16. Galassi F, Renieri G, Sodi A, et al. Nitric oxide proxies and ocular perfusion pressure in primary open angle glaucoma. Br J Ophthalmol. 2004; 88:757–60.
Article
17. Ellis DZ, Dismuke WM, Chokshi BM. Characterization of soluble guanylate cyclase in NO-induced increases in aqueous humor outflow facility and in the trabecular meshwork. Invest Ophthalmol Vis Sci. 2009; 50:1808–13.
Article
18. Mosmann T. Rapid colorimetric assay for cellular growth and survival: Application to proliferation and cytotoxicity assays. J Immunol Methods. 1983; 65:55–63.
Article
19. Green LC, Wagner DA, Glogowski J, et al. Analysis of nitrate, nitrite and [15 N]nitrate in biological fluids. Anal Biochem. 1982; 126:131–8.
20. Polansky JR, Weinreb RN, Baxter JD, Alvarado J. Human trabecular cells. I. Establishment in tissue culture and growth characteristics. Invest Ophthalmol Vis Sci. 1979; 18:1043–9.
21. Alvarado JA, Wood I, Polansky JR. Human trabecular cells. II. Growth pattern and ultrastructural characteristics. Invest Ophthalmol Vis Sci. 1982; 23:464–78.
22. Kawa JE, Higginbotham EJ, Chang IL, Yue BY. Effects of anti-glaucoma medications on bovine trabecular meshwork cells in vitro. Exp Eye Res. 1993; 57:557–65.
Article
23. Green K, Downs SJ. Ocular penetration of pilocarpine in rabbits. Arch Ophthalmol. 1975; 93:1165–8.
Article
24. Yu AL, Fuchshofer R, Kampik A, Welge-Lű ssen U. Effects of oxidative stress in trabecular meshwork cells are reduced by prostaglandin analogues. Invest Ophthalmol Vis Sci. 2008; 49:4872–80.
Article
25. Vasa M, Breitschopf K, Zeiher AM, Dimmeler S. Nitric oxide acti-vates telomerase and delays endothelial cell senescence. Circ Res. 2000; 87:540–2.
Article
26. Scalera F, Borlak J, Beckmann B, et al. Endogenous nitric oxide synthesis inhibitor asymmetric dimethyl L-arginine accelerates endothelial cell senescence. Arterioscler Thromb Vasc Biol. 2004; 24:1816–22.
Full Text Links
  • JKOS
Actions
Cited
CITED
export Copy
Close
Share
  • Twitter
  • Facebook
Similar articles
Copyright © 2024 by Korean Association of Medical Journal Editors. All rights reserved.     E-mail: koreamed@kamje.or.kr