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Biomedical subjects

W M Grant

Publications and source records attributed to W M Grant.

At least 19 recordsLinked to original sources
PubMed1979

Experimental perfusions through the anterior and vitreous chambers with possible relationships to malignant glaucoma.

Enucleated eyes were perfused alternately via the anterior and vitreous chambers. At low intraocular pressure (IOP), vitreous humor presented considerable resistance to forward flow of perfusion fluid in calf eyes, but not in human eyes. In human eyes when the perfusion pressure was increased to 60 mm Hg, the resistance to flow forward from the vitreous body increased, but became practically nil again when the IOP was decreased. At high pressure the volume of the vitreous body apparently increases and the anterior hyaloid membrane probably presses against the ciliary body, reducing the area of hyaloid membrane through which fluid can flow. Whether increased perfusion pressure can in some other manner change the permeability of human vitreous to resemble that of the calf remains unanswered. Our results suggest that factors other than, or in addition to, simple diversion of aqeous humor must be important in malignant glaucoma.

Animals↗
PubMed1979

Scanning electron microscopy of trabeculectomy specimens in open-angle glaucoma.

We examined trabeculectomy specimens obtained at the time of surgery for inadequately controlled open-angle glaucoma by scanning electron microscopy. Of the 50 specimens ten included a broad area of the trabecular meshwork. In these ten specimens the meshwork was obscured by material. We believe the degree of occlusion was significant in these specimens, which would lead to obstruction of aqueous outflow. No similar material was found in control specimens from persons of similar age.

Aged↗
PubMed1978

Thymoxamine test. Differentiating angle-closure glaucoma form open-angle glaucoma with narrow angles.

To help differentiate mild angle-closure glaucoma from open-angle glaucoma in patients with elevated intraocular pressure (IOP) and angles so narrow that the structures cannot be seen adequately, we used a thymoxamine hydrochloride eyedrop that induces miosis and tends to widen the angle. Thymoxamine does not contract the ciliary muscle and does not alter the IOP or facility of outflow in open-angle glaucoma, but it can relieve angle-closure glaucoma. A test with thymoxamine was performed in 26 patients because of this differential diagnostic dilemma. When gonioscopic, tonometric, and tonographic findings appeared to indicate a diagnosis of angle-closure glaucoma, a peripheral iridectomy was done. Subsequent (one to 27 months) observations have substantiated that testing with thymoxamine is a helpful aid in this differential diagnosis, and merits more widespread evaluation.

Adult↗
PubMed1978

A repeated dose-response study of methazolamide in glaucoma.

Twenty-two patients with open-angle glaucoma were given weekly courses of methazolamide at different dosages. Mean intraocular pressure reductions of 3.3, 4.3, and 5.6 mm Hg were achieved at dosages of 25 mg, 50 mg, and 100 mg of methazolamide every eight hours, respectively. Maximal intraocular pressure lowering was still present nine to ten hours after administration. The mean reduction in outflow pressure for all eyes receiving a daily dosage of 300 mg was only 31%, but this included eyes (17% of the total) that demonstrated less than 13% reduction in outflow pressure, despite similar methazolamide serum levels. Eight patients subsequently received acetazolamide, 250 mg four times a day for a week. The effect of this dosage of acetazolamide on pressure was between the effects of 50 and 100 mg of methazolamide three times daily.

Aged↗
PubMed1978

Serum obstruction of aqueous outflow in enucleated eyes.

We perfused enucleated human eyes via the anterior chamber by the constant pressure technique. Infusion of human serum into the anterior chamber of enucleated human eyes for 30 minutes at 23 mm Hg pressure induced a 42% decrease in facility of outflow, which was not relieved by irrigation of the anterior chamber with balanced salt solution or alpha-chymotrypsin. Diluted serum also reduced the facility of outflow. Measured in a glass viscometer, diluted serum had less viscosity than undiluted, but interfered with outflow from the eye more than anticipated on the basis of viscosity alone. When we used lens depression to induce tension on the iridocorneal angle to simulate the effects of contraction of the ciliary muscle, outflow facility increased in control eyes that had not been exposed to serum and in serum-perfused eyes. However, the partial obstruction to outflow that had been induced by serum persisted. Normal serum components may become adsorbed or entrapped in the aqueous outflow system so as to obstruct outflow, and this may result in secondary glaucoma in eyes with chronic uveitis.

Anterior Chamber↗
PubMed1978

Effects of panretinal photocoagulation on rubeosis iridis, angle neovascularization, and neovascular glaucoma.

Ninety-three patients received ruby laser panretinal photocoagulation in one eye for diabetic retinopathy and we examined them at an average time of 7.1 years later. In 14 patients, the untreated eye developed rubeosis iridis and the contralateral treated eye did not. In seven patients, the untreated eye developed angle neovascularization and the contralateral eye did not. The untreated eye developed neovascular glaucoma and the contralateral treated eye did not in four patients. Our findings suggest that eyes with proliferative retinopathy that received panretinal photocoagulation are less likely to develop rubeosis iridis, angle neovascularization, and probably neovascular glaucoma, than those eyes not receiving panretinal photocoagulation.

Adult↗
PubMed1978

Phenylephrine provocative testing in the pigmentary dispersion syndrome.

Forty-nine patients with bilateral pigmentary dispersion syndrome (abnormal accumulation of pigment in the anterior chamber, principally from the posterior layers of the iris), including 31 patients with pigmentary glaucoma, underwent 10% phenylephrine testing in one eye for evaluation of liberation of pigment floaters into the anterior chamber and the influence of phenylephrine on the intraocular pressure. Ten patients with pigmentary glaucoma developed a 3+ to 4+ pigment response, but only two demonstrated a pressure rise greater than 2 mm Hg. The highest pressure rise observed was 7 mm Hg. Nine patients with pigmentary dispersion syndrome but without glaucoma also developed a 3+ to 4+ pigment response, but none of these had a pressure rise. The incidence of pigment liberation was higher in older patients and in pigmentary glaucoma patients receiving topical antiglaucoma therapy at the time of testing. The extent of iris transillumination did not correlate with the grade of phenylephrine-induced pigment liberation. Two pigmentary glaucoma patients, who did not liberate pigment or have a pressure rise when tested with phenylephrine, did exhibit spontaneous or exercise-induced liberations of pigment into the anterior chamber, with marked rises of intraocular pressure and obstruction of aqueous outflow.

Adult↗
PubMed1978

Cyclocryotherapy of chronic open-angle glaucoma in aphakic eyes.

Twenty-six eyes of 25 patients with chronic open-angle glaucoma and surgical aphakia with inadequate control of intraocular pressure (IOP) despite maximal medical treatment were treated with cyclocryotherapy, according to a prospective protocol and specific technique. (Neovascular and synechial glaucoma were excluded from this series.) In most cases topical medications were resumed after cyclocryotherapy. During follow-up of seven to 95 months (average, 46 months), IOP was reduced to 19 mm Hg or lower in 24 out of 26 eyes (92%). In two eyes, persistent decrease in visual acuity, unrelated to reduction of IOP, occurred after cyclocryotherapy. On the basis of the long-term benefits obtained by this procedure, we concluded that cyclocryotherapy should be considered the procedure of choice in the treatment of primary open-angle glaucoma in surgically aphakic eyes when pressure cannot be adequately reduced by maximally tolerated medical treatment.

Aged↗
PubMed1978

Obstruction of aqueous outflow by lens particles and by heavy-molecular-weight soluble lens proteins.

Enucleated human eyes were perfused via the anterior chamber at 25 mm Hg pressure with lens particles (whole lens homogenates) in one series of experiments and with soluble lens proteins from human cataractous lenses in another series. Adding 1% of a homogenate of a single cataractous lens to the anterior chamber induced a 68% decrease in outflow. Perfusion with HMW soluble lens proteins (1 mg/ml; MW more than 150 million) caused a 60% decrease in outflow in 1 hr. In neither series was the obstruction to outflow relieved by subsequent irrigation of the anterior chamber with balanced salt solution or alpha-chymotrypsin. The results show that both lens particles and soluble lens proteins can directly obstruct the aqueous outflow pathways of human eyes. Such obstruction may be a significant factor in certain lens-induced glaucomas.

Aqueous Humor↗
PubMed1978

Identification of heavy-molecular-weight soluble protein in aqueous humor in human phacolytic glaucoma.

Aqueous humor was obtained by paracentesis at the time of cataract surgery from six patients with phacolytic glaucoma, diagnosed on the basis of acute unilateral open-angle glaucoma associated with an apparently leaking hypermature or mature cataract, and from six control patients with immature cataracts. Three of the latter had primary open-angle glaucoma. Quantities of heavy-molecular-weight (HMW) protein (MW greater than 150 X 10(6)) sufficient to obstruct aqueous outflow were identified in all six phacolytic aqueous humor specimens but in none of the controls. Three of the hypermature cataractous lenses from the cases of phacolytic glaucoma were also examined and were found to have 14-fold greater quantities of HMW protein in their liquefying cortex than were present in the cortex of immature cataractous lenses. These findings, correlated with experimental HMW protein perfusion studies in excised human eyes that we have already reported, strongly suggest that direct obstruction of the aqueous outflow channels by liberated HMW soluble lens protein may be a significant and previously unappreciated factor in the pathogenesis of phacolytic glaucoma.

Aqueous Humor↗
PubMed1977

The outflow tract in pigmentary glaucoma: a light and electron microscopic study.

Buttons obtained by trephination from both eyes of a 44-year-old myopic man with pigmentary glaucoma were studied by light and electron microscopy. Although clinically both eyes exhibited heavy pigmentation of the trabecular meshwork in the whole circumference, microscopically the trabecular meshwork of the left eye contained more pigment granules than that of the right eye, which appeared relatively acellular with collapse of the trabecular sheets. In both eyes endothelial cells covering the trabecular sheets were filled with pigment and showed various stages of degeneration. The intertrabecular spaces contained free pigment granules as well as cell debris. These observations suggest that plugging of the trabecular spaces by pigment and cell debris together with fragmentation and collapse of trabecular sheets contribute to the decrease in the facility of outflow that occurs in pigmentary glaucoma.

Endothelium↗
PubMed1977

Carbonic anhydrase inhibitor side effects. Serum chemical analysis.

Multiple serum chemical values were examined in 92 patients with chronic glaucoma who were treated with the carbonic anhydrase inhibitors (CAIs) acetazolamide or methazolamide, seeking relationships between serum composition and symptomatic side effects. Of the 92 patients, 44 complained of a symptom-complex of malaise, fatigue, weight loss, depression, anorexia, and loss of libido, which we have found most commonly to threaten continuation of therapy. Patients who had this symptom complex were significantly more acidotic than those without it. Ten of 24 patients who had chemical evidence of excessive acidosis reported a dramatic alleviation of symptoms when sodium bicarbonate was administered, although their serum CO2-combining power changed little. There was no correlation of the symptom complex with serum potassium concentration, except in a few patients who were simultaneously receiving chlorothiazide diuretics for systemic hypertension and who became frankly hypokalemic.

Acetazolamide↗
PubMed1977

Secondary open-angle glaucoma in histiocytosis X.

A 9 month-old boy developed secondary open-angle glaucoma associated with fever and multiple lytic bone lesions 2 1/2 months after cataract aspiration. An open bone biopsy provided a diagnosis of histiocytosis X. Hisiocytes similar to those in the bone were identified in a specimen of aqueous humor from the affected eye. No other cells were found. The abnormal histiocytes may have caused the glaucoma by infiltrating the trabecular angle structures and mechanically obstructing aqueous outflow from the eye.

Bone Diseases↗
PubMed1976

Ghost cells as a cause of glaucoma.

Clinical and investigative evidence indicated a glaucoma caused mainly by degenerated red blood cells, or ghost cells. These ghost cells, with altered shape, color, and pliability, accumulated in the vitreous cavity after hemorrhage. Following disruption of the anterior hyaloid face, they passed into the anterior chamber and caused severe glaucoma. In the anterior chamber, the tiny, khakicolored cells, circulating slowly, were frequently mistaken for white blood cells. They covered the trabecular meshwork or filled the inferior angle with a pathognomonic khaki-colored layer. They were identified by phase-contrast microscopic examination of anterior chamber aspirates. The decreased pliability of these degenerated cells seemed to account for their inability to pass easily through the human trabecular meshwork and, therefore, to cause severe glaucoma.

Aged↗