Klin Monbl Augenheilkd 2009; 226(4): 332-336
DOI: 10.1055/s-0028-1109310
Originalarbeit

© Georg Thieme Verlag KG Stuttgart · New York

Adrenaline-Induced Chronic Ocular Hypertension in Adult Rabbits

Adrenalin-induzierte chronische Augendruckerhöhung bei adulten KaninchenI. Mikheytseva1 , E. Lipovetskaya1 , O. Kopp1 , M. Mozaffarieh2 , M. C. Grieshaber2 , J. Flammer2 , P. Meyer2
  • 1The Filatov Research Institute of Eye Diseases, Odessa, Ukraine
  • 2University Eye Clinic, Basel, Switzerland
Further Information

Publication History

received: 25.9.2008

accepted: 18.12.2008

Publication Date:
21 April 2009 (online)

Zusammenfassung

Hintergrund: Beschreibung eines neuen Tiermodells zum besseren Verständnis der pathophysiologischen Mechanismen beim Glaukom. Material und Methoden: Von 40 weißen Riesenkaninchen wurden 30 Tiere behandelt, 10 Tiere dienten als Kontrollgruppe. Die Kaninchen wurden 3 Monate lang wiederholt mit Boli von Adrenalin-Hydrochlorid (0,1 mL einer 0,1 % Lösung) behandelt, welche ihnen in die Ohrvenen injiziert wurden. Die Kontrollgruppe erhielt statt Adrenalin physiologische Kochsalzlösung. Gemessen wurden der Augendruck (IOD) und die Abflussrate des Kammerwassers bei Beginn, während und nach der Behandlung (nach 4 – 6 Monaten, 7 – 9 Monaten und 10 – 12 Monaten). Ergebnisse: Im Vergleich zur Kontrollgruppe zeigten die mit Adrenalin behandelten Tiere während der Behandlung eine signifikante Steigerung des Augendrucks um 25 % und 12 Monate nach der Behandlung um 57 %. Ferner zeigte der Vergleich, dass die Abflussrate des Kammerwassers bei den behandelten Tieren um 16,5 % während der Behandlung zunahm und dann kontinuierlich um 60 % nach der Behandlung sank. Schlussfolgerungen: Das vorliegende Tiermodell dürfte für künftige Untersuchungen des Pathomechanismus beim Glaukom wertvoll sein.

Abstract

Background: The aim of this study was to develop a new animal model to enhance our understanding of the biological pathomechanisms involved in glaucoma. Materials and Methods: Forty white giant rabbits were divided into a treated (N = 30) and a control group (N = 10). Boli of adrenaline hydrochloride (0.1 mL 0.1 % solution) were repeatedly injected into the veins of the ears of the rabbits and physiological saline in the control group, respectively, for three months. Intraocular pressure (IOP) and outflow facility of the aqueous humour were measured prior to, during and after treatment (4 – 6 months, 7 – 9 months, 10 – 12 months). Results: In comparison to the control group, the adrenaline-treated group showed a significant increase in IOP both during treatment (25 %) and 12 months after treatment (57 %). Comparative analysis further showed that the aqueous humour outflow facility of the treated group increased by 16.5 % during the treatment, and showed a continuous decrease of 60 % after treatment. Conclusion: This rabbit model could be useful for further investigations of the pathomechanisms involved in glaucoma.

References

  • 1 Quigley H A. Neuronal death in glaucoma.  Prog Retin Eye Res. 1999;  18 39-57
  • 2 Weinreb R N, Lindsey J D. The importance of models in glaucoma research.  J Glaucoma. 2005;  14 302-304
  • 3 Shareef S R, Garcia-Valenzuela E, Salierno A. et al . Chronic ocular hypertension following episcleral venous occlusion in rats.  Exp Eye Res. 1995;  61 379-382
  • 4 Morrison J C. Elevated intraocular pressure and optic nerve injury models in the rat.  J Glaucoma. 2005;  14 315-317
  • 5 Morrison J C, Moore C G, Deppmeier L M. et al . A rat model of chronic pressure-induced optic nerve damage.  Exp Eye Res. 1997;  64 85-96
  • 6 Gaasterland D, Kupfer C. Experimental glaucoma in the rhesus monkey.  Invest Ophthalmol. 1974;  13 455-457
  • 7 Grozdanic S D, Betts D M, Sakaguchi D S. et al . Temporary elevation of the intraocular pressure by cauterization of vortex and episcleral veins in rats causes functional deficits in the retina and optic nerve.  Exp Eye Res. 2003;  77 27-33
  • 8 Emre M, Orgul S, Gugleta K. et al . Ocular blood flow alteration in glaucoma is related to systemic vascular dysregulation.  Br J Ophthalmol. 2004;  88 662-666
  • 9 Flammer J. Glaucomatous optic neuropathy: a reperfusion injury.  Klin Monatsbl Augenheilkd. 2001;  218 290-291
  • 10 Flammer J, Orgul S, Costa V. et al . The impact of ocular blood flow in glaucoma.  Prog Retin Eye Res. 2002;  21 359-393
  • 11 Grieshaber M C, Flammer J. Blood flow in glaucoma.  Curr Opin Ophthalmol. 2005;  16 79-83
  • 12 Brubaker R F, Gaasterland D. The effect of isoproterenol on aqueous humor formation in humans.  Invest Ophthalmol Vis Sci. 1984;  25 357-359
  • 13 Lu Y, Li M, Shen Y. The effects of epinephrine and adrenergic antagonists on adenosine 3’, 5’-monophosphate level of bovine trabecular cells in vitro.  Zhonghua Yan Ke Za Zhi. 1998;  34 124-126
  • 14 Pache M, Flammer J. A sick eye in a sick body? Systemic findings in patients with primary open-angle glaucoma.  Surv Ophthalmol. 2006;  51 179-212
  • 15 Klaver J H, Greve E L, Goslinga H. et al . Blood and plasma viscosity measurements in patients with glaucoma.  Br J Ophthalmol. 1985;  69 765-770
  • 16 Bonovas S, Filioussi K, Tsantes A. et al . Epidemiological association between cigarette smoking and primary open-angle glaucoma: a meta-analysis.  Public Health. 2004;  118 256-261
  • 17 Chisholm I A, Stead S. Plasma lipid patterns in patients with suspected glaucoma.  Can J Ophthalmol. 1988;  23 164-167
  • 18 Topouzis F, Coleman A L, Harris A. et al . Association of blood pressure status with the optic disk structure in non-glaucoma subjects: the Thessaloniki eye study.  Am J Ophthalmol. 2006;  142 60-67
  • 19 Stamer W D, Roberts B C, Howell D N. et al . Isolation, culture, and characterization of endothelial cells from Schlemm’s canal.  Invest Ophthalmol Vis Sci. 1998;  39 1804-1812
  • 20 Kobayashi T, Tahara Y, Matsumoto M. et al . Roles of thromboxane A(2) and prostacyclin in the development of atherosclerosis in apoE-deficient mice.  J Clin Invest. 2004;  114 784-794
  • 21 Nie Q, Fan J, Haraoka S. et al . Inhibition of mononuclear cell recruitment in aortic intima by treatment with anti-ICAM-1 and anti-LFA-1 monoclonal antibodies in hypercholesterolemic rats: implications of the ICAM-1 and LFA-1 pathway in atherogenesis.  Lab Invest. 1997;  77 469-482
  • 22 Smith J L. Unilateral glaucoma in carotid occlusive disease.  JAMA. 1962;  182 683-684
  • 23 Bergmanson J P. The anatomy of the rabbit aqueous outflow pathway.  Acta Ophthalmol. 1985;  63 493-501
  • 24 Nishida S, Uchida H, Takeuchi M. et al . Scanning electron microscope study of the rabbit anterior chamber angle.  Med Mol Morphol. 2005;  38 54-62
  • 25 Nakabayashi M. Ischemic hypertension of pigeon eye.  Jpn J Ophthalmol. 2001;  45 128-136
  • 26 Saxena N, Sharma M. Cerebral infarction following carotid arterial injection of adrenaline.  Can J Anaesth. 2005;  52 119
  • 27 Caspi J, Coles J G, Benson L N. et al . Effects of high plasma epinephrine and Ca2 + concentrations on neonatal myocardial function after ischemia.  J Thorac Cardiovasc Surg. 1993;  105 59-67
  • 28 Lalonde D, Bell M, Benoit P. et al . A multicenter prospective study of 3,110 consecutive cases of elective epinephrine use in the fingers and hand: the Dalhousie Project clinical phase.  J Hand Surg. 2005;  30 1061-1067
  • 29 Arfi A M, Kouatli A, Al-Ata J. et al . Acute myocardial ischemia following accidental intravenous administration of epinephrine in high concentration.  Indian Heart J. 2005;  57 261-264
  • 30 Reitsamer H A, Kiel J W. A rabbit model to study orbital venous pressure, intraocular pressure, and ocular hemodynamics simultaneously.  Invest Ophthalmol Vis Sci. 2002;  43 3728-3734
  • 31 Giuffre I, Taverniti L, Di Staso S. The effects of 2 % ibopamine eye drops on the intraocular pressure and pupil motility of patients with open-angle glaucoma.  Eur J Ophthalmol. 2004;  14 508-513
  • 32 Knepper P A, Farbman A I, Telser A G. Aqueous outflow pathway glycosaminoglycans.  Exp Eye Res. 1981;  32 265-277

Prof. Dr. Peter Meyer

Augenklinik, Universitätsspital Basel

Mittlere Straße 91

4031 Basel

Switzerland

Email: meyerpe@uhbs.ch