Purpose: Several studies have shown that administration of granulocyte-colony stimulating factor (G-CSF) is followed by an increase of white blood cell (WBC) count. There is evidence from other vascular beds that an increase in WBC count impairs blood flow regulation especially in the microcirculation. Whether this also holds true for the ocular circulation is yet unknown. In the following trial we investigated whether an increase in WBC count alters the oxygen induced vasoconstriction of retinal vessels.

Methods: The study design was randomized, double-masked, placebo-controlled with two parallel groups. 24 healthy, male subjects were included. Measurements of retinal white blood cell flux with the blue-field entoptic technique, red blood cell velocity using the laser Doppler velocimeter and retinal vessel diameter using a Retinal Vessel Analyzer, were assessed at baseline and after breathing of 100% oxygen over 20 min. Thereafter 300 μg of G-CSF or placebo was administered. Measurements were repeated after another inhalation of 100% oxygen 8h later.

Results: G-CSF did not show any influence on systemic hemodynamics. WBC count increased significantly from 5.7 ± 1.6 × 10(9)/L at baseline up to 19.5 ± 4.8 × 10(9)/L 8h after G-CSF administration. As expected, oxygen breathing induced a pronounced vasoconstriction and a decrease red and white cell flux in both, the placebo and the G-CSF group (p<0.01 for both groups). Administration of G-CSF increased WBC flux, but did not affect red blood cell flux. The response of red blood cell flux and retinal vessel diameters to hyperoxia was not altered by G-CSF administration. However, leukocytosis leads to a more pronounced oxygen induced reduction in red blood cell velocity compared to the placebo group (p=0.024).

Conclusion: Our data indicate that increased WBC count as induced with G-CSF, leads to a more pronounced reduction in retinal red blood cell flux during states of vasoconstriction. This indicates that, as in other vascular beds, an increase in WBC leads to an altered blood flow regulation.

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Source
http://dx.doi.org/10.1016/j.mvr.2011.09.007DOI Listing

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