BACKGROUND: Habitual smoking is a risk factor for a variety of vascular diseases, including ocular pathologies. In the current study, we set out to investigate whether the regulation of retinal vascular tone is impaired in habitual smokers. For this purpose, vascular reactivity was tested during flicker light induced vasodilatation in smokers and in a non-smoking control group. METHODS: In this prospective, balanced, parallel group study 24 chronic smokers (28.1 ± 3.3 years) and 24 age-matched never-smoking volunteers (28.2 ± 4.0 years) were included. Flicker induced vasodilatation was measured in major retinal arteries and veins using a retinal vessel analyzer and flicker induced changes in retinal blood velocities were assessed in retinal veins by laser Doppler velocimetry. Three flicker periods of 60s were scheduled. Blood cotinine concentration was determined and a Fagerstrom questionnaire was performed to evaluate nicotine dependency. RESULTS: In non-smoking subjects, stimulation with flicker light increased retinal venous diameter by +7.7 ± 3.1%, +6.9 ± 2.9% and +7.1 ± 2.8% during the three flicker periods, respectively. Flicker induced vasodilatation in veins was significantly diminished in chronic smokers (+4.9 ± 2.4%, +6.3 ± 3.1% and +5.7 ± 3.4%, ANOVA between groups, p=0.032) as compared to the non-smoking control group. Calculated retinal blood flow in the measured veins increased by a maximum of +54 ± 21%, +43 ± 18% and +46 ± 19% during the three stimulation periods in the non-smoking subjects, respectively. The flicker induced increase in retinal blood flow as assessed in the veins was significantly reduced in chronic smokers as compared to the non-smoking control group (+19 ± 16%, +26 ± 14%, +24 ± 13%, ANOVA between groups, p=0.013). In retinal arteries, flicker stimulation increased retinal arterial diameters by 5.2 ± 3.8%, 5.8 ± 4.8% and 5.5 ± 5.6% during the three flicker periods in the non-smoking group. In smokers, the flicker induced arterial vasodilatation was not significantly different compared to non-smokers (4.6 ± 4.1%, 3.8 ± 3.7% and 4.8 ± 3.4%, ANOVA between groups, p=0.4). CONCLUSION: Our data indicate that the flicker induced hemodynamic response of retinal veins is reduced in chronic smokers as compared to age matched healthy volunteers. This supports the hypothesis that chronic smoking leads to vascular dysfunction in the eye.
BACKGROUND: Habitual smoking is a risk factor for a variety of vascular diseases, including ocular pathologies. In the current study, we set out to investigate whether the regulation of retinal vascular tone is impaired in habitual smokers. For this purpose, vascular reactivity was tested during flicker light induced vasodilatation in smokers and in a non-smoking control group. METHODS: In this prospective, balanced, parallel group study 24 chronic smokers (28.1 ± 3.3 years) and 24 age-matched never-smoking volunteers (28.2 ± 4.0 years) were included. Flicker induced vasodilatation was measured in major retinal arteries and veins using a retinal vessel analyzer and flicker induced changes in retinal blood velocities were assessed in retinal veins by laser Doppler velocimetry. Three flicker periods of 60s were scheduled. Blood cotinine concentration was determined and a Fagerstrom questionnaire was performed to evaluate nicotine dependency. RESULTS: In non-smoking subjects, stimulation with flicker light increased retinal venous diameter by +7.7 ± 3.1%, +6.9 ± 2.9% and +7.1 ± 2.8% during the three flicker periods, respectively. Flicker induced vasodilatation in veins was significantly diminished in chronic smokers (+4.9 ± 2.4%, +6.3 ± 3.1% and +5.7 ± 3.4%, ANOVA between groups, p=0.032) as compared to the non-smoking control group. Calculated retinal blood flow in the measured veins increased by a maximum of +54 ± 21%, +43 ± 18% and +46 ± 19% during the three stimulation periods in the non-smoking subjects, respectively. The flicker induced increase in retinal blood flow as assessed in the veins was significantly reduced in chronic smokers as compared to the non-smoking control group (+19 ± 16%, +26 ± 14%, +24 ± 13%, ANOVA between groups, p=0.013). In retinal arteries, flicker stimulation increased retinal arterial diameters by 5.2 ± 3.8%, 5.8 ± 4.8% and 5.5 ± 5.6% during the three flicker periods in the non-smoking group. In smokers, the flicker induced arterial vasodilatation was not significantly different compared to non-smokers (4.6 ± 4.1%, 3.8 ± 3.7% and 4.8 ± 3.4%, ANOVA between groups, p=0.4). CONCLUSION: Our data indicate that the flicker induced hemodynamic response of retinal veins is reduced in chronic smokers as compared to age matched healthy volunteers. This supports the hypothesis that chronic smoking leads to vascular dysfunction in the eye.
Authors: Eric Wei; Yali Jia; Ou Tan; Benjamin Potsaid; Jonathan J Liu; Woojhon Choi; James G Fujimoto; David Huang Journal: PLoS One Date: 2013-12-02 Impact factor: 3.240
Authors: Ben M Sörensen; Alfons J H M Houben; Tos T J M Berendschot; Jan S A G Schouten; Abraham A Kroon; Carla J H van der Kallen; Ronald M A Henry; Annemarie Koster; Pieter C Dagnelie; Nicolaas C Schaper; Miranda T Schram; Coen D A Stehouwer Journal: PLoS One Date: 2017-10-27 Impact factor: 3.240
Authors: Frank C T van der Heide; Tan Lai Zhou; Ronald M A Henry; Alfons J H M Houben; Abraham A Kroon; Pieter C Dagnelie; Martien C J M van Dongen; Simone J P M Eussen; Tos T J M Berendschot; Jan S A G Schouten; Carroll A B Webers; Miranda T Schram; Marleen M J van Greevenbroek; Anke Wesselius; Casper G Schalkwijk; Annemarie Koster; Hans H C M Savelberg; Nicolaas C Schaper; Koen D Reesink; Coen D A Stehouwer Journal: Microcirculation Date: 2021-05-06 Impact factor: 2.628