Investigative Ophthalmology & Visual Science, Vol. 30, No. 6, June 1989
Copyright © Association for Research in Vision and Ophthalmology
Effect of Topical Timolol Maleate on the
Ophthalmic Artery Blood Pressure
Juan E. Grunwald and Candace Furubayashi
The effects of topical timolol maleate 0.5% on the ophthalmic artery diastolic (OABPd), systolic
(OABPS) and mean blood pressure (OABPm) were investigated in 19 healthy subjects using compression ophthalmodynamometry. In a randomized, double-blind study, one eye of each subject received
one drop of timolol maleate 0.5% and the fellow eye received a drop of placebo. Measurements of
OABPd and OABPS were performed just prior to instillation of the drops, and then 2 hr later. OABPm
was calculated as OABPm = OABPd + '/> (OABPS - OABPd). No significant changes in OABPd,
OABP5 or OABPm were observed following the drops in the timolol-treated eyes or in the placebotreated eyes. A significant difference (P = 0.0198) was found, however, when the changes in OABPm
occurring in the timolol-treated eyes were compared with the changes occurring in the placebo-treated
eyes, suggesting that the drug may have an effect upon ophthalmic artery pressure and retinal artery
pressure that is expressed differently in each eye. Invest Ophthalmol Vis Sci 30:1095-1100,1989
In a previous study using bidirectional laser
Doppler velocimetry and monochromatic fundus
photography, we have reported that topical timolol
maleate 0.5% produces an average increase in retinal
blood flow of 13% in the normal eye.1 Since the average increase in perfusion pressure in these eyes was
13% and since we found a significant correlation between the individual changes in blood velocity and
the changes in perfusion pressure, we concluded that
the increase in blood flow is produced by the increase
in perfusion pressure. In order to calculate perfusion
pressure, one must determine the central retinal artery blood pressure. In this previous work, however,
the central retinal artery pressure was not measured
and was estimated as % of the mean brachial artery
pressure minus the intraocular pressure (IOP).
Measurements of the human central retinal artery
blood pressure cannot be determined noninvasively
at this time. A close estimation of the blood pressure
in the ophthalmic artery pressure, which is only
slightly higher than the central retinal artery, can be
obtained, however, by compression ophthalmodynamometry. 23 To investigate whether topical timolol
maleate may have an effect on the diastolic, systolic
From the Scheie Eye Institute, Department of Ophthalmology,
School of Medicine, University of Pennsylvania, Philadelphia,
Pennsylvania.
This investigation was supported in part by a grant from Chibret
International, Merck Sharp and Dohme and was assisted by the use
of Clinfo data management and analysis provided by a grant
(RR-00040) from the NIH.
Submitted for publication: January 28, 1988; accepted December 12, 1988.
Reprint requests: Dr. Juan E. Grunwald, Scheie Eye Institute, 51
N. 39th Street, Philadelphia, PA 19104.
1095
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and mean ophthalmic artery blood pressure (OABPd,
OABPS and OABPm, respectively) we have performed
the current study in which these pressures were estimated from compression ophthalmodynamometry
measurements. Our results showed no significant
change in OABPd, OABPS or OABPm from baseline.
However, when the changes in OABPm in the timolol-treated eye were compared to the changes in the
placebo-treated eyes, a statistically significant difference between eyes was detected.
Although the effect of timolol maleate on aqueous
humor secretion and IOP has been extensively studied in the literature, very little is known about any
influence that this drug may have on the ophthalmic
and retinal artery blood pressures. The ophthalmic
artery and the extraocular part of the central retinal
artery are known to have adrenergic innervation. Although such innervation was previously believed to
be absent in the blood vessels of the mammalian retina, 45 recent reports have suggested that adrenergic
nerves are present in the rabbit.6 In addition, FerrariDileo7 has demonstrated the presence of beta adrenergic binding sites in the retinal vasculature. It is possible, therefore, that timolol maleate, which has been
shown to reach significant concentrations in the retina, sclera and possibly optic nerve following topical
instillation, could have an effect on both the ophthalmic and the retinal artery pressures.
Materials and Methods
Nineteen healthy volunteers aged 20 to 47 years
(average 28.5 ± 7.2 years, ±1 SD) with no history of
systemic or intraocular disease were included in the
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INVESTIGATIVE OPHTHALMOLOGY b VISUAL SCIENCE / June 1989
study. All eyes had a best refracted visual acuity of
6/6, an IOP of 21 mm Hg or less and a normal anterior segment and fundus. None of the subjects were
taking topical or systemic medications at the time of
the study. Informed consent was obtained from each
subject after the procedures had been fully explained.
After pupillary dilation with tropicamide 1%, the
intraocular pressure was determined by Goldmann
applanation tonometry. In a sitting position, the
heart rate was determined and the brachial artery systolic and diastolic blood pressures were measured by
sphygmomanometry using the Accutorr 1A Non-Invasive Blood Pressure Monitor (Datascope Corporation, Paramus, NJ). Following a few drops of proparacaine hydrochloride 0.5% (Alcaine, Alcon Laboratories, Fort Worth, TX) and with the subject in a
standing position, compression ophthalmodynamometry (WCO, Bradenton, FL) was performed.
One investigator observed the major retinal arteries
by direct ophthalmoscopy, while a second person
pressed on the temporal sclera by means of the
ophthalmodynamometer, and a third observer recorded the force shown by the instrument. The
ophthalmodynamometric force that resulted in the
first observed complete collapse of the retinal arteries
at the optic nerve head was determined.2'8 Two consecutive measurements were obtained and the mean
was recorded as F d . Whenever the difference between
the two consecutive force determinations was 6 g or
larger a new set of measurements was performed.
After the determination of F d , the ophthalmodynamometric force was again increased. The force
which caused a total collapse of the arteries with disappearance of pulsation was then determined.2 8 Two
consecutive measurements were obtained and the
average was recorded as F s . Whenver the difference
between the two consecutive determinations was 10 g
or larger, a new set of measurements was performed.
All three subjects measuring Fd and F s were masked
with regard to which eye had received timolol. The
investigator performing direct ophthalmoscopy was
also masked with regard to the values of Fd and Fs
obtained.
In a double-masked randomized design, one eye of
each subject received one drop of timolol maleate
0.5% ophthalmic solution, and the fellow eye received one drop of placebo consisting of the vehicle of
timolol ophthalmic solution. To maximize the intraocular penetration of the drugs, the drops were
instilled over the cornea. Two hours later, the experimental procedure was repeated. Subjects were asked
to refrain from eating or drinking during this time.
Mean ophthalmodynamometric force (Fm) was
calculated as Fm = Fd + '/? (Fs - Fd). Diastolic, systolic
and mean ophthalmic artery blood pressure (OABPd,
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Vol. 30
OABPS and OABPmj respectively) were determined
from the values F d , F s and F m and the resting IOP
using Table 9 of Weigelin et al,2 which provides estimates of the ophthalmic artery pressure based on the
ophthalmodynamometric force and a range of resting
IOPs.
Mean brachial artery blood pressure, BP m , was
considered as: BPm = BPd + Vi (BPS - BPd), where BPS
and BPd are the brachial artery systolic and diastolic
pressures.
Statistical evaluation of the data was performed
using paired student t-test (two-tailed), linear regression and correlation analysis. Prior to this, the presence of a normal distribution of the data was assessed
by the Wilk-Shapiro normality test. Findings with an
error probability smaller than 0.05 were considered
as statistically significant. Results are presented as
means ± one standard deviation.
Results
Measurements of mean brachial artery blood pressure, heart rate and IOP are shown in Table 1. Following treatment, there was no significant change in
diastolic (from 58.9 ± 7.8 mm Hg to 58.8 ± 7.7 mm
Hg), systolic (from 112.0 ± 12.1 mm Hg to 108.3
± 12.2 mm Hg) or mean (from 76.6 ± 8.8 mm Hg to
75.3 ± 8.4 mm Hg) brachial artery blood pressures.
Heart rate, however, decreased significantly from an
average of 73.5 ± 7.3 to 66.7 ± 9.6 (paired student
t-test, P = 0.0002) (Table 1).
Intraocular pressure decreased from an average of
15.1 ± 2.7 mm Hg to 9.3 ± 2.0 mm Hg (P = 0.0001)
in the timolol-treated eyes, and from an average of
14.6 ± 2.5 mm Hg to 11.5 ± 2.1 mm Hg (P = 0.0001)
in the eyes that received placebo (Table 1). The average decrease in IOP was significantly larger in the
timolol-treated eyes than in the fellow eyes (P
= 0.001).
The values of the F d , Fs and F m in each eye before
and after the instillation of placebo and timolol drops
are presented in Table 2. In the timolol eyes, significant increases of 4.8 ± 7.2 gram (P = 0.0099) in F d , of
5.4 ± 9.5 gram (P = 0.0245) in F s , and of 5.0 ± 5.9
gram (P = 0.0016) in F m were found when the
changes in the timolol-treated eyes were compared
with the changes in the placebo-treated eyes.
When the changes in the timolol-treated eyes were
analyzed separately, significant increases from baseline in average Fd (4.5 ± 6.6 gram, P = 0.0077) and
F m (3.5 ± 6.4 gram, P = 0.0278) were observed following the drops. There was a 1.3 ± 9.6 gram increase
in Fs that was not statistically significant.
In the placebo-treated eyes, no statistically significant changes from baseline in average Fd (—0.3 ± 6.2
No. 6
EFFECT OF TIMOLOL ON OPHTHALMIC ARTERY DLOOD PRESSURE / Grunwold and Furubayashi
1097
Table 1. Measurements of heart rate, mean brachial artery blood pressure (BPm) and intraocular pressure (IOP)
IOP (mmHg)
Subject #
1 Before
After
2 Before
After
3 Before
After
4 Before
After
5 Before
After
6 Before
After
7 Before
After
8 Before
After
9 Before
After
10 Before
After
11 Before
After
12 Before
After
13 Before
After
14 Before
After
15 Before
After
16 Before
After
17 Before
After
18 Before
After
19 Before
After
Age
(years)
Sex
Eye
Heart rate
27
M
OD
71
64
63
53
69
57
75
68
65
73
68
61
39
M
OS
41
M
OD
29
F
OD
26
M
OS
29
M
OS
26
M
OS
68
52
24
M
OS
34
F
OS
81
76
66
62
78
62
88
81
89
89
78
65
76
78
76
68
72
59
74
62
74
72
66
66
21
F
OD
21
F
OD
27
F
OD
25
M
OS
20
F
OD
26
M
OD
21
F
OS
OS
30
F
47
F
OS
28
F
OD
gram, P = 0.8553) or F m (-1.5 ± 6.3, P = 0.3110)
were observed. A marginally significant decrease in
average F s from baseline (-4.0 ± 8.2 gram, P
= 0.0482) was present.
As described before, the OABP d , OABPS and
OABPm were calculated from the determinations of
F d , Fs and F m , respectively, taking into account the
resting IOP (Table 3). No statistically significant
changes in OABPd, OABPS or OABPm were found in
the timolol-treated eyes or in the placebo-treated
eyes. Following the instillation of drops, however,
there was a statistically significant difference of 3.1
± 5.2 mm Hg (P = 0.0198) between the changes in
OABPm observed in the timolol-treated eyes and
those observed in the placebo-treated eyes. This was
due to an average increase of 0.5 ± 5.5 mm Hg (P
= 0.7103) in OABPm in the timolol-treated eyes and
an average decrease of - 2 . 6 ± 5 . 4 mm Hg (P
= 0.0527) in the placebo-treated eyes. No statistically
significant differences between the changes in OABPd
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BPm
(mmHg)
Placebo
Timolol
14
11
12
10
12
10
12
12
13
9
12
10
11
9
16
12
17
12
17
12
14
11
16
12
16
12
14
14
10
12
5
13
9
14
11
12
8
12
7
11
7
16
8
79
68
79
77
79
73
79
69
71
84
87
90
87
87
92
82
67
65
75
64
87
78
78
82
73
83
56
59
82
75
72
79
78
78
65
65
70
72
8
10
19
12
14
9
16
12
16
9
14
8
8
21
17
15
10
15
13
13
14
18
13
21
13
16
9
15
9
14
11
19
9
or OABPS observed in the timolol-treated eyes and
those observed in the placebo-treated eyes were detected following the instillation of the drops.
No significant correlations were found between the
changes in blood pressure or IOP and the changes in
F d , Fs and F m . Also, no significant correlations were
detected between the changes in blood pressure or
IOP and the changes in OABPd, OABPS and OABPm.
Discussion
Compression ophthalmodynamometry is a technique in which the direct observation of the collapse
of the central retinal artery under increased intraocular pressure is used to determine the pressure in the
ophthalmic artery. Although the collapse of the central retinal artery is monitored as an end point, the
measurements obtained reflect the pressure somewhere in the course of the ophthalmic artery, between
its origin from the internal carotid and its end at the
1098
Vol. 30
INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE / June 1989
Table 2. Measurements of ophthalmodynamometnc diastolic (Fd), systolic (Fs) and mean (Fm) force
before and after the instillation of placebo and timolol
Fd\ 'gram)
F; (gram)
Subject #
Placebo
Timolol
Placebo
1 Before
After
2 Before
After
3 Before
After
4 Before
After
5 Before
After
6 Before
After
7 Before
After
8 Before
After
9 Before
After
10 Before
After
11 Before
After
12 Before
After
13 Before
After
14 Before
After
15 Before
After
16 Before
After
17 Before
After
18 Before
After
19 Before
After
27
36
21
16
19
28
33
34
21
16
36
35
43
38
27
31
32
23
23
15
40
50
34
33
25
27
23
21
34
31
28
39
21
15
22
19
23
20
22
32
23
26
21
33
28
32
23
21
24
43
34
43
22
38
22
26
21
14
53
56
32
31
26
31
15
20
26
29
26
27
23
24
28
23
26
32
89
87
72
66
69
85
87
76
71
58
84
77
82
72
63
69
89
70
66
64
103
104
78
73
76
73
65
73
96
89
90
93
63
51
82
76
central retinal artery.2 This method is clinically used
as an aid in the diagnosis of carotid artery occlusive
disease.
Compression ophthalmodynamometry provides
an estimate of the diastolic and systolic forces (F d , F s ,
respectively) needed to reach the diastolic and systolic end points. The results of this study show that
topical timolol maleate significantly increases F d , the
ophthalmodynamometric force needed to reach the
diastolic end point. F m , which is calculated from Fd
and F s , is also significantly increased following the
instillation of timolol.
To determine the ophthalmic artery pressure, however, it is important to know not only the ophthalmodynamometnc force, but also the resting IOP. In
an eye with lower IOP more force will be needed to
reach the end point than in an eye with higher IOP.
The above-mentioned increase in Fd is probably due
in part to the fact that timolol decreases IOP. Since
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68
61
Fm (gram)
Timolol
75
87
72
64
68
76
90
89
60
59
85
88
63
67
58
63
81
74
77
68
98
130
78
79
68
67
70
77
87
82
74
74
62
61
90
79
76
74
Placebo
Timolol
48
53
38
33
36
47
51
48
38
30
52
49
56
49
39
44
51
39
37
31
61
68
49
46
42
42
37
38
55
40
50
39
39
37
47
49
51
35
34
44
58
44
51
34
46
42
42
40
32
68
81
47
47
40
43
50
49
33
39
46
47
42
57
35
27
42
38
38
34
43
36
36
49
42
42
46
the IOP is lower after timolol treatment, a greater
force must be applied on the eye to reach the
OABPd ? To compensate for the effect of a change in
IOP on the estimation of the ophthalmic artery pressure based on the ophthalmodynamometric force, we
have used Table 9 of Weigelin et al,2 which provides
estimates of the ophthalmic artery pressure based on
the ophthalmodynamometric force and a range of
resting IOPs. In the interpretation of our results we
have assumed that these published data are correct.
When the OABPd, OABPS and OABPm are calculated from F d , Fs and F m , taking into account the
resting IOP of the measured eyes,2 there are no statistically significant differences from baseline in the timolol- or the placebo-treated eyes.
A comparison of the changes in OABPm that occur
in the timolol-treated eyes with the changes in
OABPm that occur in the placebo-treated eyes shows,
however, a statistically significant average difference
No. 6
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EFFECT OF TIMOLOL ON OPHTHALMIC ARTERY BLOOD PRESSURE / Grunwald and Furubayashi
Table 3. Measurements of the ophthalmic artery diastolic (OABPd), systolic (OABPS) and mean (OABPm)
blood pressure before and after the instillation of placebo and timolol
OABPS
(mm Hg)
OABPd
(mm Hg)
Subject #
1 Before
After
2 Before
After
3 Before
After
4 Before
After
5 Before
After
6 Before
After
7 Before
After
8 Before
After
9 Before
After
10 Before
After
11 Before
After
12 Before
After
13 Before
After
14 Before
After
15 Before
After
16 Before
After
17 Before
After
18 Before
After
19 Before
After
Placebo
42
50
36
31
34
41
47
48
.37
31
49
47
54
50
43
45
48
38
40
32
54
61
49
47
41
41
39
35
52
47
43
51
38
32
38
35
40
36
Timolol
Placebo
38
45
38
38
37
45
43
45
38
35
39
53
47
53
39
50
40
40
39
30
65
65
47
45
42
43
32
34
45
44
42
40
39
37
43
37
44
44
96
93
81
75
78
91
34
84
81
67
91
84
89
79
74
78
67
80
78
75
109
108
87
82
86
82
76
80
106
97
97
98
74
63
90
85
80
72
of 3.1 mm Hg between eyes (P = 0.0195). This difference is due to the addition of a non significant decrease in average OABPm in the placebo-treated eyes
to a nonsignificant increase in OABPm in the timolol-treated eyes, suggesting a different effect of the
drug in the timolol-treated eyes and the placebotreated eye.
The analysis of these results is somewhat complicated by the fact that there is probably an effect of the
drug on the placebo-treated eyes, as demonstrated by
the significant decrease in IOP observed in these eyes.
Topical timolol instilled in one eye is known to produce a decrease in IOP in the contralateral eye. This
phenomenon has been described previously9"" and is
probably due to an influence of the drug reaching the
fellow eye through the systemic circulation. In addition, timolol lowers the heart rate and the systemic
blood pressure,12 thus affecting the circulation of
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OABPm
(mm Hg)
Timolol
84
93
81
71
78
83
97
95
70
68
92
92
70
74
70
71
91
82
90
77
104
130
87
87
79
75
81
83
98
90
84
81
73
70
97
86
87
81
Placebo
Timolol
61
63
51
46
49
58
62
60
52
43
63
60
54
61
52
49
51
57
62
62
48
46
56
66
56
60
49
66
59
53
56
64
52
52
46
72
77
62
58
56
55
51
50
70
64
62
67
50
42
55
52
53
48
56
57
54
56
46
78
87
60
59
54
54
48
50
62
59
56
54
50
48
62
54
58
56
both the timolol- and the placebo-treated eyes. We
would like to stress, therefore, that although we describe eyes as placebo-treated eyes, these eyes are
most probably affected by the timolol delivered in the
fellow eye.
A different concentration of the drug in each eye
and possibly each retrobulbar tissue could perhaps
explain the difference in OABPm changes observed
between eyes. Previous studies of timolol penetration
in the rabbit eye following instillation have indeed
shown concentrations of the drug that were several
times higher in the sclera, retina and choroid of the
treated eye than in plasma.13 The concentrations of
the drug in the fellow eye that received timolol
through the circulation were probably much lower
than those achieved in the instilled eye.
Although only a speculation at this time, we would
like to present another mechanism that could explain
1100
INVESTIGATIVE OPHTHALMOLOGY G VISUAL SCIENCE / June 1989
our results. Topical timolol maleate is known to produce a systemic effect resulting in decreases of blood
pressure and heart rate.12 Such decreases would cause
a decrease in OABPm that would be of similar magnitude in both eyes. A simultaneous effect of the drug in
the timolol-treated eyes leading to vasodilatation of
the ophthalmic artery could prevent such decrease in
OABPm in these eyes and result in the significant
difference in the change in OABPm observed between
eyes.
In our previous study1 in which OABPm was assumed to be % of BP m , we estimated an average increase in perfusion pressure of 13% in the timololtreated eyes and of 7% in the placebo-treated eyes.
This corresponded to a difference of 6% in the change
in perfusion pressure between eyes. According to the
results of our current study, and using a more accurate determination of perfusion pressure (PP) based
on the formula: PP = OABPm - IOP, we have calculated that perfusion pressure actually increases by an
average of 15 ± 13% in the timolol-treated eyes and
only by 1 + 13% in the placebo-treated eyes, corresponding to a difference of 14% in the changes in
perfusion pressure between eyes. Interestingly, these
average percentage changes in perfusion pressure are
very similar to our previously reported average
changes in blood flows of 1.5% in the placebo-treated
eyes and of 13% in the timolol-treated1 eyes.
Pillunat et al14 have measured the effect of timolol
maleate on the "systolic retinal perfusion pressure"
by a method described by Ulrich et al.15 In this
method, the IOP is raised and then slowly decreased
by a suction cup. The pressure at which oscillations in
intraocular blood volume produced by the oscillation
in blood pressure first become apparent is considered
as the "systolic retinal perfusion pressure." The results of our study are similar to those of Pillunat et al,
who found no significant change from baseline in the
"systolic perfusion pressure" following timolol treatment. Measurements of diastolic or mean pressures
and comparisons of the changes occurring between
the two eyes of each subject were not performed by
these authors.
To study whether the changes in OABP following
the instillation of the drugs were larger in eyes that
showed larger drops in IOP or in subjects that had
larger changes in systemic blood pressure, we looked
at the correlations between these quantities. No statistically significant correlations between these quantities were observed.
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Vol. 30
The technique of ophthalmodynamometry is not
very widely used today because of a generalized impression that it is not a very accurate method. The
results of this study show, however, that when carefully performed in a group of cooperative subjects,
this technique can detect small changes of ophthalmic artery blood pressure.
Key words: ophthalmic artery blood pressure, compression
ophthalmodynamometry, timolol maleate, human retina
Acknowledgment
The authors thank Sharon Grunwald for the statistical
analysis of the data, Joan Baine for technical help, and
Dolly Scott for the preparation of the manuscript.
References
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4. Cohen Al: Ultrastructural aspects of the human optic nerve.
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5. Laties AM: Central retinal artery innervation: Absence of
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6. Furukawa H: Autonomic innervation of preretinal blood vessels of the rabbit. Invest Ophthalmol Vis Sci 28:1752, 1987.
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9. Katz IM, Hubbard WA, Getson AJ, and Gould AL: Intraocular pressure decrease in normal volunteers following timolol
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