Transient Increase In Intraocular Pressure Research Articles

Prostaglandin mediated inflammatory changes induced by ?-adrenoceptor stimulation in the sympathectomised rabbit eye

Topical application of 50 microliter of 0.1% noradrenaline or 10% phenylepherine to either a surgically sympathectomised or a guanethidine treated rabbit eye induced a transient increase in intraocular pressure (IOP), between 90 and 150 min, followed by a fall to hypotensive levels. These changes were accompanied by the development of conjunctival and anterior uveal hyperemia and an aqueous flare. Fluorescein angiography and microscopic examination after intravenously injecting colloidal carbon showed that the major site of disruption of the blood-aqueous barrier occurs in the ciliary processes. Slightly elevated levels of protein and prostaglandin-like activity (PG) were detected in aqueous samples withdrawn 3 or 5 h after application of either adrenergic agent. Prior treatment with indomethacin or phentolamine prevented the ocular hypertensive phase as well as the inflammatory changes, suggesting that the inflammatory rebound is mediated by PG and that PG release under such circumstances is closely linked to alpha-adrenoceptor activation. By contrast, the rise in IOP occurring after each of several successive daily applications of an alpha-agonist to a normal rabbit eye was not accompanied by hyperemia or an aqueous flare and was not inhibited by indomethacin pretreatment.

Die Blockade sekund�rer Drucksteigerungen nach Cyclokryocoagulation

Prostaglandin mediated transient increase in intraocular pressure following cryokoagulation of the ciliary body in rabbits was completely inhibited by preoperative administration of Aspisol (D, L-Lysin-mono-(acetylsalicylat)). To avoid additional increase in intraocular pressure in patients chosen for cyclocryotherapy, pretreatment with Aspisol could prove to be effective.

Adrenergic drugs and intraocular pressure: Effects of selective β-adrenergic agonists

Changes in intraocular pressure and pupil diameter were studied in rabbits following topical administration of relatively selective and non-selective adrenergic agonists. Drugs having strong α-adrenoceptor stimulating effects (norepinephrine, phenylephrine, epinephrine) initially produced a transient increase in intraocular pressure and pupil diameter before eliciting any ocular hypotensive effects. In contrast, those drugs with predominately β-adrenoceptor stimulating properties (isoproterenol, isoetharine, metaproterenol, terbutaline, salbutamol, carbuterol) produced an immediate decrease in intraocular pressure without causing ocular hypertension or mydriasis. Significantly, the decreases in intraocular pressure were more pronounced with those drugs having strong β 2-adrenoceptor stimulating activity. Thus, stimulation of α- and β-adrenoceptors can produce opposite initial effects on intraocular pressure, but α-adrenergic mechanisms may interact with β 1- and/or β 2-adrenoceptor mechanisms to produce subsequent ocular hypotension. Most importantly these data indicate that more selective β 2-adrenoceptor stimulation is an effective mechanism for lowering intraocular pressure.

The comparative short-term mammalian toxicology of phenarsazine oxide and phenoxarsine oxide.

Phenoxarsine oxide (PXO) and phenarsazine oxide (PZO) are organic arsenicals used as industrial biocides. The acute LD50 (in mg kg-1) for PZO was 83 (rat) and 77 (guinea pig) and for PXO 40 (rat) and 24 (guinea pig). PXO was more irritant to the gastrointestinal tract. Liver pathology did not occur in PZO-guinea pigs, but PZO was more hepatotoxic than PXO in rats. The acute inhalation L (ct)50 values were 12830 mg min m-3 for PXO and 13650 mg min m-3 for PZO in guinea pigs; death was due to asphyxia. The guinea pig acute L(ct)50 given as a divided dose over 30 days to guinea pigs and rats did not produce toxic signs, but mononuclear cell infiltration of the portal tracts occurred. PXO and PZO were found to be primary skin and eye irritants; PXO produced more severe effects. The no-effect concentration for keratitis with solutions was 0.25% PZO and 0.1% PXO; both compounds caused concentration dependant transient increases in intraocular pressure, the proportionate increases being significantly greater with PXO. Thus, although PXO and PZO are equitoxic by acute inhalation, PXO is more toxic orally and more irritant to the skin, eye and gastrointestinal tract but PZO is more hepatotoxic.

Complicated retinal detachment and its management with pars plana vitrectomy.

Fifty patients with retinal detachment accompanied by vitreous haemorrhage, perforating eye injuries, intraocular foreign bodies, massive preretinal retraction,.giant tears greater than 180 degrees, and proliferative retinopathies underwent pars plana vitrectomy, cryocoagulation, scleral buckling, and intravitreal gas injection. Intraoperative complications included minimal to moderate bleeding and iatrogenic retinal tears, but no retinal dialysis was produced at the pars plana sclerotomy site. Postoperative complications included recurrent vitreous haemorrhage, rubeosis, haemolytic, erythroclastic, or neovascular glaucoma, transient increase of intraocular pressure, uveitis, and macular pucker. Phthisis bulbi occurred in 6 eyes; in 3 of these eyes enucleation was required. Successful reattachment was accomplished in 56% of these complicated retinal detachments, most of which had been considered inoperable by conventional techniques. Visual improvement was achieved in 46% of eyes. Follow-up ranged from 6 to 29 months.

The effects of external ocular irritation on intraocular pressure.

Riot control agents (tear gases) cause intense eye irritation and reflex squeezing of the eyes. The intraocular pressure under these circumstances is unknown but animal and human studies of ocular irritation and forces acting upon the eye indicate a transient increase in intraocular pressure which is not necessarily detrimental to vision.

Aspirin prevents the disruption of the blood-aqueous barrier in the rabbit eye.

THE acutely traumatized mammalian eye shows an irritative response, characterized by hyperaemia of the conjunctiva and iris, miosis, disruption of the blood–aqueous barrier, and a transient increase in intraocular pressure followed by relative hypotony. One sign of the disruption of the barrier is a positive aqueous flare, with increased concentrations of blood proteins in the aqueous humour. Stimuli that elicit all or part of this response in the rabbit eye include nitrogen mustard instillation in the conjunctival sac1, subcutaneous injection of melanocyte stimulating hormone (MSH)2, stroking the iris3,4 or cornea5, infrared irradiation of the iris6, mechanical stimulation of the trigeminal nerve7, and anterior chamber paracentesis8.

Aphakic flat anterior chamber. Treatment by anterior vitriotomy.

Twenty eyes with an flat anterior chamber syndrome were identified among the complications of 8,533 cataract surgeries. This syndrome of aphakic pupillary-block flat anterior chamber treatable by anterior vitriotomy consisted of (1) flat and shallow anterior chamber; (2) vitreous pupillary and iridectomy block; (3) fixed pupil; (4) lack of response to topically applied mydriatics, acetazolamide, or osmotic agents; (5) transient increase in intraocular pressure to levels of 20 mm Hg or higher; (6) lack of deepening of the anterior chamber after iridectomy, iridotomies, reformation of the anterior chamber with saline or air, or vitreous aspirations; (7) immediate deepening of the anterior chamber following anterior vitriotomy.