2.2 The effect of hypoxia on visual function
2.2.6 The effect of hypoxia on dark adaptation
The effect of hypoxia on dark adaptation has been recognised since the 1930s, with early studies finding that dark adapted thresholds were elevated in response to hypoxia, but that the time taken for DA to occur seemed not to be affected (McFarland et al. 1939; McDonald and Adler 1939; Wald and Harper 1942a). McFarland and Evans (1939) and McDonald and Adler (1939) both found an elevation of 0.40 log units in absolute threshold with hypoxia in both the rod and cone systems, whilst the rate of dark
adaptation appeared unchanged. Data collected from 20 subjects in the McFarland and Evans (1939) study, showed that rod photoreceptors were more sensitive to the
reduction in oxygen tension.
Figure 2-4 shows the mean adaptation curves of six subjects under reduced oxygen concentrations, ranging from 21% to 10.1% (McFarland & Forbes, 1940), and
demonstrates raised dark adapted thresholds under hypoxic conditions. The data show that the thresholds for rod and cones were elevated, with the scotopic threshold ranging from 2.85 to 3.05 log microlamberts in the control series, to 3.50 to 3.85 log
microlamberts when breathing 10.1% oxygen. It can also be seen that the curves are parallel with the control curves, showing the time course remained unaffected. Both McFarland and Evans (1939) and Mcfarland and Forbes (1940) found that, at the end of
the experiment when 100% oxygen was supplied to the subjects, the sensitivity increased rapidly. This led to the conclusion that the effect of hypoxia upon the dark adaptation function was not related to regeneration of visual pigment, as the recovery was too rapid, but instead to the neural retina and the central nervous system. This theory was also supported by the finding that reduced oxygen had a greater effect at lower light intensities (Hecht and Hendley 1946).
Figure 2-4. Mean dark adaptation curves for 6 subjects under various oxygen tensions. (McFarland and Forbes. 1940).
One recent study has found the time course of dark adaptation to be affected by hypoxia (Connolly et al. 2006). By studying dark adaptation using fixed stimulus intensities and measuring time as the dependent variable, recovery post bleach of both the cone and rod thresholds was recorded. As can be seen in Figure 2-5 the rod cone break was delayed
participants were at simulated 4572m (12% oxygen) when compared to the dark adaptation curves obtained at ground level. However this study did not evaluate quantitative measures of adaptation, such as the time constants of rod and cone recovery.
Figure 2-5. Effect of hypoxia when breathing air at 4572m on the rate of dark
adaptation in 5 subjects showing detection time displacement relative to a control dark adaptation breathing air at ground level Connolly and Hosking (2006).
When comparing their results with the earlier findings of no change in the time course of the rod, cone or rod cone break portions of the curve, it seemed possible that the rod cone break in the earlier studies may have been missed by infrequent measurements of threshold. Connolly and Hosking (2006) discussed that if the rod cone break was inferred in the absence of data points, it could mean that the rod section of the curve may have
actually included data from the cone portion of the curve, masking the delay in the rod cone break and shifting the rod section to the right.
The effects of high altitude/ reducing oxygen concentration on thresholds have been found to be rapid and transient (Kobrick et al 1984; Wald & Harper, 1942). Wald and Harper (1942) found that the threshold adjusts rapidly (within 1-10 minutes) to hypoxia (8-11% oxygen), with exposures lasting five to six hours not translating to greater or more persistent changes. The results from Ernst and Krill (1971) indicated that the first four minutes of rod and cone adaptation were not affected by hypoxia, and concluded that this was due to this section relating to neural rather than photochemical processes. This hypothesis is in contrast to McFarland and Evans (1939), McFarland and Forbes (1940), McDonald and Adler (1939) and Hecht and Hendley (1946) who all concluded that the effect of hypoxia on dark adaptation was not related to photochemical processes but rather to neural processes. Kobrick et al. (1984), found that the major effect of hypoxia was in the first 10 minutes and suggested that the differences found could be due to the longer duration of hypoxia in their study.
Several studies have used hypoxia induced by disease to study the dark adaptation process. Thylefors et al. (2009) assessed dark adaptation in patients with respiratory insufficiency, all of which were on long-term oxygen therapy (for at least 4 months) when breathing their normal oxygen dose, and when they had been without it for at a mean of 4 hrs. They found no change in the dark adaptation function without oxygen, despite a
due to the lack of hypocapnia that would, at high altitudes in a normal population, cause vasoconstriction and reduce not only the concentration of oxygen but also its delivery. The subjects in their study were hypercapnic or normocapnic so may have larger blood vessel lumens, which would be further dilated during hypoxia, therefore preserving dark adaptation.
In conclusion, dark adaptation has been shown to be affected by hypoxia, with current evidence suggesting that it affects both final threshold and the rate of dark adaptation.