Jacob Bell
New Member
John C. Merritt, MD
Chapel Hill, North Carolina
The glaucomas are characterized by increased
intraocular pressure resulting in damage to the optic
nerve. Concomitant ocular pathology that can
frequently result in increased pressures are due to:
(1) fibrovascular membranes; (2) inflammatory
closure by synechiae; (3) trauma, either social or
surgical; (4) trabecular obstruction (blood, macrophages,
alpha-chymatrypsin); (5) lens-induced
glaucomas; and (6) corneal endotheliopathy-atrophic
iris syndromes. The primary glaucomas are
either of the open or closed-angle varieties. Primary
open-angle glaucoma, the most common variety,
is characterized by (1) increased pressures
within the eye (increased ocular tension, OT); (2)
pressure-related visual field defects1' 2; and (3) optic
nerve pallor and atrophy.
No good epidemiological data exist on the prevalence
ofopen-angle glaucoma. In 1978 a cohort study
from Framingham, Massachusetts, suggested that
3 percent of this 99.4 percent Caucasian population
has open-angle glaucoma.3 Although there are
no data on blacks, the National Eye Institute suggested
that data retrieved from a model reporting
area (22 states in 1970) suggested that open-angle
glaucoma blinded three to five times more nonwhites
than whites.4
Open-angle glaucoma treatment traditionally
has been medical in the United States. Data gathered
over ten years in Cambridge, England, have
inferred that primary surgical interventions may
be more effective in open-angle glaucoma.5 The
medical therapies include eye drops (miotics, aqueous
inflow inhibitors) and systemic carbonic anhydrase
inhibitors. Topical beta adrenergic blockers
(timolol), epinephrine and its pro-drug (dipivefrin
hydrochloride) all lower ocular tension by decreasing
aqueous formation. The miotics, however,
lower ocular tension by increasing aqueous outflow
from the anterior chamber. Blacks respond
less favorably to miotics,6'7 epinephrine8 and
timolol,9 than whites. Similarly, surgical procedures
designed to lower ocular tension by aqueous
drainage from the anterior chamber (filtering
operations) have significantly higher failure and
complication rates among blacks than in
whites. 1012 Therefore, any ocular hypotensive
agent should receive clinical trials not only in
these various types of glaucomas, but also in various
population subsets.
Mexican marijuana, containing 1.8 to 2.8 percent
A9 tetrahydrocannabinol (A9 THC), has consistently
been shown to lower both intraocular
pressure and blood pressure in both open-angle
glaucoma13 and heterogenous glaucoma.14'15 The
decreased ocular tension results from decreased
aqueous production mediated through the pressuredependent
portion of aqueous formation (ultrafiltration).
Characteristically, marijuana induces a
tachycardia within 5 to 10 minutes, which is invariably
followed by decreased blood and intraocular
pressures. The maximum ocular hypotensive effect
of 25 to 30 percent occurs between 60 and 90
minutes.
Cardiovascular changes generally return to
baseline with 3'/2 hours; but ocular hypotensive
responses often persist longer.15 Sudden precipitous
falls in systolic blood pressure have occurred
in 18 percent of marijuana-naive subjects inhaling
Mexican marijuana. These syncopal-like episodes
were characterized by sudden falls in blood pressure,
lightheadedness, a faint, and thready pulse
often accompanied by nausea and bradycardia.
Positioning the subject in a reclining position invariably
alleviated these signs. This postural hypotension
was not related to plasma A9 THC levels,
previous marijuana experience, or inhalation
techniques.16 A similar episode of postural hypotension
and dysphoria occurred 1 hour after the
ingestion of 5 mg of oral A9 THC in a 52-year-old
black woman with both essential hypertension and
open-angle glaucoma. Although our studies would
indicate that 5 mg of oral A9 THC are inactive in
heterogenous glaucoma, this case may represent a
certain sensitivity of the hypertensive glaucoma patient
to the peripheral dilatory effects of A9 THC. 17
Hypertensive subjects have consistently been
shown to receive a more substantial lowering of
the blood pressure and intraocular pressure when
compared to normotensive glaucoma populations.
18'19 Similarly, topical 0.1 percent A9 THC in
light mineral oil vehicles decreased the systolic
blood pressure 12.8 mmHg (in 8 hypertensive glaucoma
subjects) after unilateral topical applications.
19 The maximum hypotensive effect in both
treated and untreated eyes after unilateral topical
A9 THC has repeatedly been shown to occur at 6
hours with significant ocular hypotensive effects
persisting for 8 to 12 hours in both animal and
human studies.19'20 It is known that the contralateral
decrease of ocular tension in fellow untreated
eyes after topical A9 in light mineral oil vehicle
results from decreased aqueous production.21 Less
well demonstrated are the possible cardiac and/or
central nervous system mechanisms involved in
aqueous dynamics. Systemic A9 THC therapies
invariably produce a decreased perfusion pressure
to the eye. This decreased perfusion to an already
damaged optic nerve may not be of long-term
benefit to glaucoma victims, although it may
well treat their concomitant essential hypertension.
Therefore, other cannabinoids which may
exert a pressure-lowering effect locally within the
eye should become the focus of present glaucoma
research.
Literature Cited
1. Armaly MF. The visual field defect and ocular pressure
level in open-angle glaucoma. Invest Ophthalmol
1969; 8:105-124.
2. Heilmann K. On the reversibility of visual field defects
in glaucomas. Trans Am Acad Ophthalmol Oto 1974;
78:304-308.
3. Kini MM, Leibowitz HM, Colton T, et al. Prevalence
of senile cataract, diabetic retinopathy, senile macular degeneration
and open angle glaucoma in the Framingham
Eye Study. Am J Ophthalmol 1978; 85:28-34.
4. Moorhead HB, Kahn HA. Statistics on blindness in
Model Reporting Area, 1969-1970. DHEW (NIH) 73-417.
Government Printing Office, 1973.
5. Watson PG, Grierson I. The place of trabeculectomy
in treatment of glaucomas. Ophthalmology 1981; 88:175-
196.
6. Krill AE, Newell FW. Effects of pilocarpine on ocular
tension dynamics. Am J Ophthalmol 1964; 57:34-41.
7. Harris LS, Galin MA. Effect of ocular pigmentation
on ocular tension dynamics. Am J Ophthalmol 1971; 72:
923-925.
8. Melikian HE, Lieberman TW, Leopold IH. Ocular
pigmentation and pressure outflow response to pilocarpine
and epinephrine. Am J Ophthalmol 1971; 72:70-73.
9. Katz IM, Berger ET. Effects of iris pigmentation on
response of ocular pressure to timolol. Surv Ophthalmol
1979; 23:395-398.
10. Welsh NH. Failure of filtration operations in Africans.
Br J Ophthalmol 1970; 54:594-598.
1 1. Merritt JC. Filtering procedures in American blacks.
Ophthalmol Surg 1980; 11:91-94.
12. Miller RD, Barber JC. Trabeculectomy in black patients.
Ophthalmol Surg 1981; 12:46-50.
13. Merritt JC, Crawford WJ, Alexander PC, et al. Effect
of marihuana inhalation on the intraocular pressure and
blood pressure in open angle glaucoma. Ophthalmology
1979; 86:45.
14. Crawford WJ, Merritt JC. Effect of tetrahydrocannabinol
on arterial and intraocular hypertension. Int J Clin
Pharmacol Biopharm 1979; 17:191-196.
15. Merritt JC, Crawford WJ, Alexander PC, et al. Effect
of marihuana inhalation on intraocular and blood pressure
in glaucoma. Ophthalmology 1980; 86:222-228.
16. Merritt JC, Cooke EC, Davis KH. Orthostatic hypotension
after A9 tetrahydrocannabinol marihuana inhalation.
(In press-Ophthalmic Research).
17. Merritt JC, McKinnon SM, Armstrong JR, et al. Effect
of oral A9 tetrahydrocannabinol in heterogenous glaucomas.
Ann Ophthalmol 1980; 12:947-950.
18. Crawford WJ, Alexander PC, Merritt JC, et al. Tetrahydrocannabinol
effect on elevated blood pressure in humans.
Prev Med 1978; 7:54.
19. Merritt JC, Olsen JL, Armstrong JR, et al. Topical A9
tetrahydrocannabinol in hypertensive glaucomas. J Pharm
Pharmacol 1981; 33:40-41.
20. Merritt JC, Peiffer RL, McKinnon SM, et al. Effect of
topical A9 tetrahydrocannabinol on intraocular pressure in
dogs. Glaucoma 1981; 3:13-16.
21. Merritt JC, Perry DD, Russell DM. Topical A9 tetrahydrocannabinol
(A9 THC) and aqueous dynamics in glaucoma.
J Clin Pharmacol 1981; 21:467S-471S.
Source: Glaucoma, Hypertension, And Marijuana
Chapel Hill, North Carolina
The glaucomas are characterized by increased
intraocular pressure resulting in damage to the optic
nerve. Concomitant ocular pathology that can
frequently result in increased pressures are due to:
(1) fibrovascular membranes; (2) inflammatory
closure by synechiae; (3) trauma, either social or
surgical; (4) trabecular obstruction (blood, macrophages,
alpha-chymatrypsin); (5) lens-induced
glaucomas; and (6) corneal endotheliopathy-atrophic
iris syndromes. The primary glaucomas are
either of the open or closed-angle varieties. Primary
open-angle glaucoma, the most common variety,
is characterized by (1) increased pressures
within the eye (increased ocular tension, OT); (2)
pressure-related visual field defects1' 2; and (3) optic
nerve pallor and atrophy.
No good epidemiological data exist on the prevalence
ofopen-angle glaucoma. In 1978 a cohort study
from Framingham, Massachusetts, suggested that
3 percent of this 99.4 percent Caucasian population
has open-angle glaucoma.3 Although there are
no data on blacks, the National Eye Institute suggested
that data retrieved from a model reporting
area (22 states in 1970) suggested that open-angle
glaucoma blinded three to five times more nonwhites
than whites.4
Open-angle glaucoma treatment traditionally
has been medical in the United States. Data gathered
over ten years in Cambridge, England, have
inferred that primary surgical interventions may
be more effective in open-angle glaucoma.5 The
medical therapies include eye drops (miotics, aqueous
inflow inhibitors) and systemic carbonic anhydrase
inhibitors. Topical beta adrenergic blockers
(timolol), epinephrine and its pro-drug (dipivefrin
hydrochloride) all lower ocular tension by decreasing
aqueous formation. The miotics, however,
lower ocular tension by increasing aqueous outflow
from the anterior chamber. Blacks respond
less favorably to miotics,6'7 epinephrine8 and
timolol,9 than whites. Similarly, surgical procedures
designed to lower ocular tension by aqueous
drainage from the anterior chamber (filtering
operations) have significantly higher failure and
complication rates among blacks than in
whites. 1012 Therefore, any ocular hypotensive
agent should receive clinical trials not only in
these various types of glaucomas, but also in various
population subsets.
Mexican marijuana, containing 1.8 to 2.8 percent
A9 tetrahydrocannabinol (A9 THC), has consistently
been shown to lower both intraocular
pressure and blood pressure in both open-angle
glaucoma13 and heterogenous glaucoma.14'15 The
decreased ocular tension results from decreased
aqueous production mediated through the pressuredependent
portion of aqueous formation (ultrafiltration).
Characteristically, marijuana induces a
tachycardia within 5 to 10 minutes, which is invariably
followed by decreased blood and intraocular
pressures. The maximum ocular hypotensive effect
of 25 to 30 percent occurs between 60 and 90
minutes.
Cardiovascular changes generally return to
baseline with 3'/2 hours; but ocular hypotensive
responses often persist longer.15 Sudden precipitous
falls in systolic blood pressure have occurred
in 18 percent of marijuana-naive subjects inhaling
Mexican marijuana. These syncopal-like episodes
were characterized by sudden falls in blood pressure,
lightheadedness, a faint, and thready pulse
often accompanied by nausea and bradycardia.
Positioning the subject in a reclining position invariably
alleviated these signs. This postural hypotension
was not related to plasma A9 THC levels,
previous marijuana experience, or inhalation
techniques.16 A similar episode of postural hypotension
and dysphoria occurred 1 hour after the
ingestion of 5 mg of oral A9 THC in a 52-year-old
black woman with both essential hypertension and
open-angle glaucoma. Although our studies would
indicate that 5 mg of oral A9 THC are inactive in
heterogenous glaucoma, this case may represent a
certain sensitivity of the hypertensive glaucoma patient
to the peripheral dilatory effects of A9 THC. 17
Hypertensive subjects have consistently been
shown to receive a more substantial lowering of
the blood pressure and intraocular pressure when
compared to normotensive glaucoma populations.
18'19 Similarly, topical 0.1 percent A9 THC in
light mineral oil vehicles decreased the systolic
blood pressure 12.8 mmHg (in 8 hypertensive glaucoma
subjects) after unilateral topical applications.
19 The maximum hypotensive effect in both
treated and untreated eyes after unilateral topical
A9 THC has repeatedly been shown to occur at 6
hours with significant ocular hypotensive effects
persisting for 8 to 12 hours in both animal and
human studies.19'20 It is known that the contralateral
decrease of ocular tension in fellow untreated
eyes after topical A9 in light mineral oil vehicle
results from decreased aqueous production.21 Less
well demonstrated are the possible cardiac and/or
central nervous system mechanisms involved in
aqueous dynamics. Systemic A9 THC therapies
invariably produce a decreased perfusion pressure
to the eye. This decreased perfusion to an already
damaged optic nerve may not be of long-term
benefit to glaucoma victims, although it may
well treat their concomitant essential hypertension.
Therefore, other cannabinoids which may
exert a pressure-lowering effect locally within the
eye should become the focus of present glaucoma
research.
Literature Cited
1. Armaly MF. The visual field defect and ocular pressure
level in open-angle glaucoma. Invest Ophthalmol
1969; 8:105-124.
2. Heilmann K. On the reversibility of visual field defects
in glaucomas. Trans Am Acad Ophthalmol Oto 1974;
78:304-308.
3. Kini MM, Leibowitz HM, Colton T, et al. Prevalence
of senile cataract, diabetic retinopathy, senile macular degeneration
and open angle glaucoma in the Framingham
Eye Study. Am J Ophthalmol 1978; 85:28-34.
4. Moorhead HB, Kahn HA. Statistics on blindness in
Model Reporting Area, 1969-1970. DHEW (NIH) 73-417.
Government Printing Office, 1973.
5. Watson PG, Grierson I. The place of trabeculectomy
in treatment of glaucomas. Ophthalmology 1981; 88:175-
196.
6. Krill AE, Newell FW. Effects of pilocarpine on ocular
tension dynamics. Am J Ophthalmol 1964; 57:34-41.
7. Harris LS, Galin MA. Effect of ocular pigmentation
on ocular tension dynamics. Am J Ophthalmol 1971; 72:
923-925.
8. Melikian HE, Lieberman TW, Leopold IH. Ocular
pigmentation and pressure outflow response to pilocarpine
and epinephrine. Am J Ophthalmol 1971; 72:70-73.
9. Katz IM, Berger ET. Effects of iris pigmentation on
response of ocular pressure to timolol. Surv Ophthalmol
1979; 23:395-398.
10. Welsh NH. Failure of filtration operations in Africans.
Br J Ophthalmol 1970; 54:594-598.
1 1. Merritt JC. Filtering procedures in American blacks.
Ophthalmol Surg 1980; 11:91-94.
12. Miller RD, Barber JC. Trabeculectomy in black patients.
Ophthalmol Surg 1981; 12:46-50.
13. Merritt JC, Crawford WJ, Alexander PC, et al. Effect
of marihuana inhalation on the intraocular pressure and
blood pressure in open angle glaucoma. Ophthalmology
1979; 86:45.
14. Crawford WJ, Merritt JC. Effect of tetrahydrocannabinol
on arterial and intraocular hypertension. Int J Clin
Pharmacol Biopharm 1979; 17:191-196.
15. Merritt JC, Crawford WJ, Alexander PC, et al. Effect
of marihuana inhalation on intraocular and blood pressure
in glaucoma. Ophthalmology 1980; 86:222-228.
16. Merritt JC, Cooke EC, Davis KH. Orthostatic hypotension
after A9 tetrahydrocannabinol marihuana inhalation.
(In press-Ophthalmic Research).
17. Merritt JC, McKinnon SM, Armstrong JR, et al. Effect
of oral A9 tetrahydrocannabinol in heterogenous glaucomas.
Ann Ophthalmol 1980; 12:947-950.
18. Crawford WJ, Alexander PC, Merritt JC, et al. Tetrahydrocannabinol
effect on elevated blood pressure in humans.
Prev Med 1978; 7:54.
19. Merritt JC, Olsen JL, Armstrong JR, et al. Topical A9
tetrahydrocannabinol in hypertensive glaucomas. J Pharm
Pharmacol 1981; 33:40-41.
20. Merritt JC, Peiffer RL, McKinnon SM, et al. Effect of
topical A9 tetrahydrocannabinol on intraocular pressure in
dogs. Glaucoma 1981; 3:13-16.
21. Merritt JC, Perry DD, Russell DM. Topical A9 tetrahydrocannabinol
(A9 THC) and aqueous dynamics in glaucoma.
J Clin Pharmacol 1981; 21:467S-471S.
Source: Glaucoma, Hypertension, And Marijuana
