Disease relevance of Ocular Hypotension

• Thus the 1,11-lactone and 11,15-dipivaloyl ester prodrugs appeared to be superior to the others in providing bioavailable PGF2alpha for ocular hypotension, while minimizing hyperemia [1].
• These injections resulted in uveitis characterized by prolonged ocular hypotony, increased protein concentrations and decreased ascorbic acid concentrations in both the vitreous and aqueous humors, and an apparent decrease in the transport function of the anterior uvea [2].
• Although PGF2 alpha and, to a much lesser extent, PGE2 have a miotic effect in cats, PGs of the A and B type did not cause significant miosis even at doses 50- to 100-fold greater than the minimum dose required to yield significant ocular hypotension [3].
• On the basis of our results, we believe that a causal relationship exists between the metabolic acidosis induced by acetazolamide, and by other drugs that have a blood-acidifying effect as the result of other mechanisms, and ocular hypotension, bothin the animal and in the glaucomatous patient [4].
• However, because of the limited drug-induced ocular hypotension, brimonidine should be combined with other drugs when used for the glaucomas in the dog [5].

High impact information on Ocular Hypotension

• This indicates that brimonidine has a neuroprotective activity unrelated to its effect on ocular hypotension [6].
• By contrast, adding CO2 sufficient to maintain isocapnic conditions (experimental end-tidal PCO2 = 38.9 versus 38.5 mm Hg in the control study; P = not significant) abolished the exercise-induced ocular hypotension (experimental IOP = 17.8 versus 18.1 mm Hg in the control study; P = not significant) [7].
• Prostaglandin D2 (PGD2) exerts a variety of biologic actions in the eye; these include ocular hypotension and inflammatory effects on the conjunctiva [8].
• Ocular hypotension in the rabbit. Receptor mechanisms of pirbuterol and nylidrin [9].
• However, pretreatment with spiperone, a D(2) receptor antagonist, did not affect the 7-OH-DPAT-induced ocular hypotension [10].

Chemical compound and disease context of Ocular Hypotension

• Pilocarpine antagonizes prostaglandin F2 alpha-induced ocular hypotension in monkeys. Evidence for enhancement of Uveoscleral outflow by prostaglandin F2 alpha [11].
• Isobutylmethylxanthine enhances adrenergic-induced ocular hypotension in rabbits and beagles [12].
• These findings suggest that 2-alkynyladenosine derivatives may affect intraocular pressure via adenosine A2 receptor, and 2-alkynyladenosine derivative-induced ocular hypotension is due to the increase of outflow facility [13].
• DPAT-induced ocular hypotension was inhibited by pretreatment with spiroxatrine, a 5-HT(1A)and alpha(2C)receptor antagonist, but not spiperone, a 5-HT(2A)receptor antagonist [14].
• When IBMX was combined with nE or Epi the ocular hypotension in rabbits and beagles increased [12].

Anatomical context of Ocular Hypotension

• 1) The imidazoline, moxonidine (MOX), injected icvt into the anterior lateral ventricle of NZW rabbits induced ocular hypotension (> 7.0 mmHg) that persisted for two hrs [15].
• The ocular hypotension induced by adenosine agonists is consistent with the activation of adenosine A1 receptors and may involve the modulation of cAMP levels in the iris/ciliary body [16].
• RESULTS: After the glucose load, there was an increase in plasma glucose level and the level of plasma osmosis, ocular hypotension, a myopic change in refractive power, shallowing of the anterior chamber, and a thickening of the lens [17].

Gene context of Ocular Hypotension

• CONCLUSIONS: Severe atrophy of the iris stroma, retinal detachment of the posterior pole, serous detachment of the ciliary body, and ocular hypotony may occur in chronic phase of VKH disease [18].

Analytical, diagnostic and therapeutic context of Ocular Hypotension

• In non-pigmented rabbits, the ocular hypotension induced by topical administration of 7-OH-DPAT (75 microg) with CAP (115 microg) was more pronounced and sustained than that of 7-OH-DPAT without CAP [19].
• METHODS: In ten patients with ocular hypotony, an ibopamine 2% solution or placebo eyedrop was administered at 8 am and frequent applanation tonometry was performed during 10 hours on 2 days, 2 weeks apart [20].
• In initial experiments involving microinjection into the lateral ventricle, UK-14,304-18 evoked ocular hypotension that was inhibited by the alpha 2-antagonist rauwolscine but not by the I1-receptor antagonist efaroxan [21].
• Possibility of isoproterenol therapy with soft contact lenses: ocular hypotension without systemic effects [22].

References