May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Effect of endotoxin on retinal erythrocyte and leukocyte flux in healthy humans.
Author Affiliations & Notes
  • S. Lung
    of Clinical Pharmacology, University of Vienna, Vienna, Austria
  • J. Kolodjaschna
    of Clinical Pharmacology, University of Vienna, Vienna, Austria
  • F. Berisha
    of Clinical Pharmacology, University of Vienna, Vienna, Austria
  • E. Polska
    of Clinical Pharmacology, University of Vienna, Vienna, Austria
  • B. Jilma
    of Clinical Pharmacology, University of Vienna, Vienna, Austria
  • M. Wolzt
    of Clinical Pharmacology, University of Vienna, Vienna, Austria
  • L. Schmetterer
    of Clinical Pharmacology, University of Vienna, Vienna, Austria
  • Footnotes
    Commercial Relationships  S. Lung, None; J. Kolodjaschna, None; F. Berisha, None; E. Polska, None; B. Jilma, None; M. Wolzt, None; L. Schmetterer, None.
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 2608. doi:
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      S. Lung, J. Kolodjaschna, F. Berisha, E. Polska, B. Jilma, M. Wolzt, L. Schmetterer; Effect of endotoxin on retinal erythrocyte and leukocyte flux in healthy humans. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2608.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: The LPS model has provided a unique means to study mechanisms of inflammation in humans and has provided novel information regarding the interactions of inflammatory mediators and cell activation. The early phase of inflammation is characterized by leukocyte infiltration into tissues, especially neutrophils. The aim of the present study was two fold: On the one hand the hypothesis that the infliltration of leukocytes can be quantified with the blue–field entoptic technique. On the other hand a potential retinal vasodilator effect of LPS was studied by investigating retinal erythrocyte flux Methods: Measurements were done with the blue field entoptic system to assess white blood cell density and white blood cell velocity in perifoveal capillaries, with a retinal vessel analyzer to assess retinal arterial and venous diameters (n=6), with a bi–directional laser Doppler velocimeter to assess red blood cell velocities in retinal veins (n=6). In addition, blood pressure, pulse rate, intraocular pressure and leukocyte counts (n=6) were measured. All measurements were done before and 4 hours after administration of LPS. Results: LPS caused an increase in retinal venous diameters, but did not change red blood cell velocities. Accordingly, there was a small but significant increase in red blood cell flux (21%, p=0,024). White blood cell velocity did not change, but white blood cell density showed a pronounced increase (42%, p=0,023). This increase in white blood cell density was highly correlated with the increase in peripheral leukocyte count (r=0,87; p=0,023). Conclusions: The data of the present study indicate a small increase in red blood cell flux in the retina after LPS administration due to a hither unidentified mechanism. Activation of the nitric oxide system, increase in circulating catecholamines and oxidative stress are potential mediators of this effect. In addition, the present study indicates that the increase in white blood cell density is an adequate indicator of leukocyte infiltration in the human LPS model.

Keywords: blood supply • retina • inflammation 
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