Near-infrared LDF, with either a modified fundus camera
18 or a confocal optical arrangement,
15 has demonstrated its capability to quantify the response of subfoveal ChBF to various physiological stimuli. Thus, studies have assessed the effect on this flow of acute increases
19 in the IOP, increases in systemic blood pressure caused by static
20 21 22 dynamic exercises,
23 and light–dark transitions.
24 The compactness and low weight of the confocal LDF flowmeter made it possible to connect this device to the tilting table and to place it directly in front of the subject’s eye, allowing measurements to be made continuously during tilting.
Tilting the body from standing to supine changed the systemic parameters in accordance with previously reported findings.
3 9 Quantitatively, the decrease in BP
dias of 7.4% is similar to the 6.6% found by Evans et al.
11 and the 4.4% reported by Sayegh and Weigelin.
3 Confirming previous findings, we found no change in BP
syst. The 15.8% decrease in heart rate in our study (82–69 bpm) is practically identical with that found by James and Smith
13 (70–59 bpm) but larger than the 10.3% and 7.9% reported by Savin et al.
10 (77–69 bpm) and Evans et al.
11 (76–70 bpm), respectively. The differences between our study and the data of others are, most probably, only of statistical nature.
Regarding the IOP, Kothe
9 has summarized the changes in IOP occurring between upright and supine obtained by previous investigators. These changes ranged from 0.5 to 4.4 mm Hg. Thus, the average 4-mm Hg increase observed in our subjects lies within this range.
According to Friberg et al.
25 this increase in IOP between standing and supine postures appears to be closely related to increased venous pressure in the orbit and possibly to increased choroidal blood volume. This increase in volume may not translated into an increase in ChBVol, because it probably occurs in the large vessels rather than in the choriocapillaris—the region sampled by LDF.
Our results demonstrate a significant increase in the blood volume at recovery. The reason for this increase is not clear. Longer measurements during recovery may help determine the duration of this effect and whether it is due to some spatial redistribution of blood after the decrease in IOP on the return to the standing position.
The tilting of the body from standing to supine increased ChBF by an average of 11%. This increase was mainly due to a statistically significant 8% change in the velocity. This flow increase was entirely reflected in the increase of the nonpulsatile component of the flow. For each LDF parameter, the change in the pulsatile component was not significant, most probably because this component is much smaller than the nonpulsatile component, resulting in a greater variability of its measurement. The reason for this is that the LDF signal originates predominantly from the choriocapillaris,
18 where pulsatility is markedly attenuated compared with that in the choroidal arteries.
Pulsatile ocular blood flow, as measured by POBF, decreases from the seated to the supine position.
12 13 26 Based on data compiled by Kothe,
9 we calculated a mean decrease of pulsatile ocular blood flow of 19% ± 5% from the standing or sitting to the supine posture. We presume, as mentioned before, that the pulsatile component of ChBF in our measurement was too low (11.2%) to reveal such an effect. By comparison, the POBF technique is based on the pulsatility in the large vessels which is markedly higher than in the choriocapillaris. Thus, based on the value of the resistance index (RI; [(peak systolic velocity – peak diastolic velocity)/peak systolic velocity]) of 0.68 that was found by Kaiser et al.
27 in the short and long posterior ciliary arteries, we estimated that the pulsatile component of the velocity in these vessels is approximately 55% of the mean velocity.
James and Smith
13 have assumed that the decrease in pulsatile ocular blood flow is associated with an increase of the nonpulsatile part. Our results confirm this increase in nonpulsatile flow, which is primarily due to an increase in velocity. An increase in velocity was also observed in the ophthalmic artery by Doppler ultrasonography.
12
Mean ocular perfusion pressure is defined as OPP
m = OABP
m − IOP, where OABP
m is the mean ophthalmic artery pressure. In this study, OABP
m was not measured. Therefore, to assess OPP
m in standing and supine postures, we used values of OABP
m based on previous studies, involving postural changes, but where ophthalmodynamometric measurements were performed in healthy volunteers under these conditions. From the data of two studies of Sayegh and Weigelin
3 28 performed on a total of 254 normal volunteers, we derived a relationship between OABP
m and BP
m. In upright position OABP
m = 0.74 · BP
m, and in supine position OABP
m= 0.84 · BP
m. Applying these values to our BP
m and IOP data, we obtain OPP
m= 57 mm Hg in the standing and 63.6 mm Hg in the supine position—that is, an increase in OPP
m of 11.6% between these two postures. This value is very similar to the 11% change observed in our study and suggests some passive response of ChBF to the increase in OPP
m.
Bill
29 has theoretically assessed the expected OPP
m in the standing and supine positions in normal subjects. From his analysis, OPP
m= BP
m − ΔP
f − ΔP
h − IOP. ΔP
f is the loss of pressure (assumed by Bill to be 5 cm H
2O, i.e., approximately 4 mm Hg), because of the flow resistance of the vessels between the heart and the eye. ΔP
h is the static pressure difference of a water column with a height equal to the distance between the heart and the eye (assumed by Bill to be 40 cm, i.e., 29 mm Hg). The BP
m and IOP data in Bill’s study, when converted were 103 and 13 mm Hg, respectively, in upright posture and 96 and 14.8 mm Hg, respectively in the supine position (eyes 10 cm above the level of the heart). These values result in a change in OPP
m between upright and supine from 57 to 70 mm Hg (i.e., an increase of 23%).
Applying this analysis to our data and taking into account that in our test, in the supine position, the eyes were approximately 3 cm below the heart (which reduces the OABPm by approximately 4 mm Hg, instead of the 7 mm Hg in Bill’s analysis), we found that OPPm = 59 mm Hg in the standing and 79 mm Hg in the supine position—that is, an increase of approximately 34%.
If Bill’s model were representative of the events occurring in the body, the change in ChBF of only 12% in the face of a 34% increase in OPP
m would inevitably lead to the conclusion that an active mechanism is operating to increase choroidal vascular resistance to maintain ChBF in the supine posture close to that in standing position. The ophthalmodynamometric data of Sayegh and Weigelin,
3 however, suggest that some compensatory mechanism is already acting between the heart and the eye to buffer most of the increase in the blood pressure induced by the tilting from upright to supine. This could occur in the ophthalmic artery or even at the level of the internal and common carotid arteries.
10
In conclusion, our results show that mean subfoveal ChBF increases significantly (by an average of 11%) when the body is tilted from upright to supine position. This increase, which is primarily due to the nonpulsatile component of this flow, results from an increase in blood velocity. Because experimental data indicate that the ocular perfusion pressure increases by a similar percentage, which is less than expected based on purely hydrostatic considerations (Bill’s model), the response of subfoveal ChBF can be explained by the passive response of the choroidal vascular system to postural change.
The authors thank Dominique Fournier, radiologist, for the opportunity to use the tilting table.