Search PubMed⌕ Search

Biomedical subjects

D S Hull

Publications and source records attributed to D S Hull.

At least 55 records · Page 3Linked to original sources
PubMed1982

Chlorpromazine-induced corneal endothelial phototoxicity.

Chlorpromazine, which has been used extensively for the treatment of psychiatric disorders, is known to accumulate in the posterior corneal stroma, lens, and uveal tract. Because it is a phototoxic compound, the potential exists for it to cause cellular damage after light exposure. Specular microscopic perfusion of corneal endothelial cells in darkness with 0.5 mM chlorpromazine HCl resulted in a swelling rate of 18 +/- 2 micrometer/hr, whereas corneas exposed to long-wavelength ultraviolet light for 3 min in the presence of 0.5 mM chlorpromazine swelled at 37 +/- 9 micrometer/hr (p less than 0.01). Preirradiation of 0.5 mM chlorpromazine solution with ultraviolet light for 30 min and subsequent corneal perfusion with the solution resulted in a corneal swelling rate of 45 +/- 19 micrometer/hr. Cornea endothelial cells perfused with 0.5 mM chlorpromazine that was preirradiated with ultraviolet light showed marked swelling on scanning electron microscopic examination, whereas those perfused with nonirradiated chlorpromazine were flat and showed a normal mosaic pattern. Combining either 500 U/ml catalase or 290 U/ml superoxide dismutase with chlorpromazine did not alter photoinduction of corneal swelling. The data suggest that corneal endothelial chlorpromazine phototoxicity is secondary to cytotoxic products resulting from the photodynamically induced decomposition of chlorpromazine and is not caused by hydrogen peroxide or superoxide anion generated during the phototoxic reaction.

Animals↗
PubMed1981

Photodynamic alteration of cornea endothelium. Relation to bicarbonate fluxes and oxygen concentration.

Corneas were mounted in flux chambers and endothelial bicarbonate fluxes were determined following sensitization of endothelial cells with 5 . 10(-6) M rose bengal and exposure to light. Corneas exposed to light demonstrated an increased passive bicarbonate flux compared to corneas not photosensitized. Active bicarbonate flux was reduced after 5 min of light exposure, but not after 1 min of light exposure. The increase in passive bicarbonate flux was prevented by the addition of 200 microgram/ml catalase to the bathing solution; however, catalase had no effect on the photodynamic alteration of active flux. Neither 10 mM ascorbic acid nor 1.012 gram/l glutathione prevented the photodynamically induced increase in passive flux. Perfusion of corneas with 5 . 10(-6) M rose bengal dissolved in a sucrose-substituted Krebs-Ringer bicarbonate solution with a PO2 of 124 +/- 4.0 mmHg and exposed to light swelled at rates more rapid than corneas treated in a similar fashion but perfused with a solution with a PO2 of 20 +/- 4.6 mmHg. This study demonstrated that photodynamically induced corneal endothelial cell alteration results in increased passive bicarbonate flux, a time-dependent decrease in active bicarbonate flux, is oxygen dependent, and is at least in part secondary to H2O2 produced by the dismutation reaction of the superoxide free radical.

Animals↗
PubMed1981

Hydrogen peroxide and corneal endothelium.

Because of recent evidence of low levels of hydrogen peroxide in the aqueous humor, studies were performed to determine levels of corneal endothelial toxicity as well as factors modifying toxicity. Perfusion of cornea endothelial cells for 3 h with varying concentrations of hydrogen peroxide demonstrated a threshold of toxicity at a concentration between 0.3 and 0.5 mM H2O2. The toxic effect resulted in rapid corneal swelling as well as disruption of endothelial cell cytoplasm and organelles. Both the physiologic and anatomic toxic effects of 0.5 mM H2O2 could be blocked with 5400 U/ml catalase. Exposure of corneas to 20 mM H2O2 for 10 min in the presence of EDTA - Fe+3 resulted in an enhancement of corneal swelling rate more rapid than that which resulted from a 10 min exposure to 20 mM H2O2 alone. Neither the presence of ascorbic acid nor the absence of glutathione and adenosine had and effect on the cornea swelling rate which occurred during a 3 h perfusion of endothelium with 0.3 mM H2O2. Chelated iron had no effect on the corneal swelling induced by phototactivation of rose bengal presensitized cornea endothelial cells.

Animals↗
PubMed1981

Rose bengal induced corneal swelling: relation to inciting wavelength.

Cornea endothelial cells sensitized with rose bengal and exposed to light demonstrated a wavelength dependent alteration in physiological response. Corneas exposed to 549 millimicron swelled at rates similar to controls exposed to identical energy levels of incandescent light. Corneas exposed to 451, 500, 612, and 651 millimicron swelled at rates less rapid than corneas exposed to similar energy levels of incandescent light. The photodynamically induced physiological alteration of cornea endothelial cells approximately paralleled the spectral curve of rose bengal with its peak at 550 millimicron.

Animals↗
PubMed1981

A simple technique for extracapsular lens extraction in the rabbit.

The aphakic rabbit is a useful model for studying the ocular penetration and pharmacological action of topically applied drugs at the posterior pole, but the use of this model is complicated by the need for specialized preparative surgery. This paper describes a simplified procedure for planned extracapsular lens surgery which utilizes inexpensive instruments commonly available in an ophthalmology department or ophthalmic research laboratory.

Animals↗
PubMed1980

Pseudomonas pseudomallei in an anopthalmic orbit.

A 21-year old man sustained multiple facial fractures and skin lacerations during an automobile accident, with resultant necrosis of the left upper eyelid and exposure of the cornea. Bacterial and secondary fungal corneal ulceration and perforation occurred, leading to enucleation. Cultures from the noninfected anophthalmic orbit approximately eight weeks after enucleation yielded Pseudomonas pseudomallei. This is the second isolate of this domallei. This is the second isolate of this organism in the United States and the first apparent association with the ocular adnexa.

Accidents, Traffic↗
PubMed1980

Chlorhexidine effects on corneal epithelium and endothelium.

Chlorhexidine digluconate, a soft contact lens disinfectant, was perfused over rabbit corneal peithelial and endothelial surfaces under a variety of concentrations and conditions. Without protein in the bathing solutions, the cornea swelled when chlorhexidine concentrations of 20 microgram/mL or greater were perfused over the endothelium. Scanning electron microscopy demonstrated rounded, swollen cells with loss of microvilli. Perfusion of the epithelium with chlorhexidine in protein-free Ringer's solution resulted in a dose-dependent sloughing of cells and loss of microvilli, which resulted in little or no swelling when the endothelium was concomitantly bathed with oil. Corneal swelling followed at concentrations of 500 and 1,000 microgram/mL when both corneal surfaces were bathed with protein-free Ringer's solution and the epithelium was perfused with chlorhexidine. With protein included in the bathing solution, no swelling occurred when separate chlorhexidine (500 microgram/mL) and albumin (1%) solutions were applied simultaneously to the epithelial surface of corneas, with the endothelial surface bathed in Ringer's solution.

Animals↗
PubMed1980

Effect of urokinase on corneal endothelium.

Urokinase in concentrations ranging from 1,000 to 5,000 units/mL was used to perfuse the corneal endothelium of rabbits for three hours in the specular microscope. No notable corneal swelling was noted, and the corneal endothelium appeared normal when observed with scanning electron microscopy.

Animals↗
PubMed1979

Influence of cetylpyridinium chloride on corneal permeability to penicillin.

The epithelial surface or the deepithelialized anterior stromal surface of isolated rabbit corneas was perfused for 3 hr with 14C-penicillin in 25 mM Ringer-bicarbonate solution with or without 1% albumin and with or without 0.02% cetylpyridinium chloride. The intact epithelium acted as a barrier to penicillin and impeded the flux rate by 66% when compared to the flux rate across the deepithelialized cornea. The presence of 0.02% cetylpyridinium chloride increased the penicillin flux rate across corneas with an intact epithelial layer to that of deepithelialized corneas. Cetylpyridinium chloride, 0.02%, had no effect on penicillin flux across deepithelialized corneas. The penicillin flux rate across corneas, with or without epithelium, was increased slightly following the inclusion of 1.0% albumin in the bathing solution. The flux rates across deepithelialized corneas in the presence of albumin, with or without cetylpyridinium chloride, were similar to fluxes found in the absence of albumin. Albumin-penicillin "binding" was not a significant factor in impeding penicillin flux, and this binding apparently was not altered by cetylpyridinium chloride. The surfactant appeared to alter epithelial permeability physiologically.

Animals↗
PubMed1979

Effects of epinephrine, benzalkonium chloride, and intraocular miotics on corneal endothelium.

Drugs formulated for use both inside and outside of the eye were tested for their potential toxic effects on the corneal endothelium. Commercially available epinephrine 1:1000 was toxic to the corneal endothelium, but solutions diluted fivefold caused no endothelial damage. The toxic agent was the sodium bisulfite 0.1% preservative. Benzalkonium chloride is highly toxic to corneal endothelium in its commonly used concentration of 0.01% and had to be diluted one thousand times to prevent endothelial damage. Ophthalmic medications for extraocular use should never be used intracamerally. Miotics commonly used in surgery during intraocular lens implantation are generally nontoxic to the cornea, though caution is advised in the use of carbachol in patients with preexisting endothelial disease and in patients having procedures in which substantial mechanical trauma to the endothelium may occur.

Animals↗
PubMed1979

Tranexamic acid and corneal deturgescence.

Recent work has demonstrated decreased corneal thickness in patients with Fuch's dystrophy and in patients following cataract extraction who were given systemic acid. Although tranexamic acid is a known antifibrinolytic drug its mechanism in reducing corneal thickness is not known. This experiment demonstrated no increase in the rate of corneal deturgescence of swollen rabbit corneas in the specular microscope when they were perfused for three h with 1 mM or 10 mM tranexamic acid. Pre-treatment of rabbits with intravenous tranexamic acid for three days and subsequent perfusion of corneas with tranexamic acid 10 mM also did not increase the rate of corneal deturgescence when compared with controls.

Animals↗
PubMed1979

Photodynamically induced alteration of cornea endothelial cell function.

Corneal endothelial cells were perfused in the specular microscope with varying concentrations of rose bengal. Corneas perfused with rose bengal in concentrations of 10(-6)M to 10(-5)M and exposed to light for periods of 0.5 to 5 min swelled at rates which were more rapid with both increasing concentration of rose bengal and increasing duration of light exposure. Corneas perfused with similar concentrations of rose bengal but not exposed to light did not swell. Combining rose bengal with 100 micrograms/ml superoxide dismutase did not reduce the corneal swelling following exposure to light, indicating that the photodynamically induced endothelial bengal perfusing solution eliminated corneal swelling following exposure of corneas to light. This indicates that the photodynamic effect of endothelium is secondary to cell functional alterations from the hydrogen peroxide produced during the dismutation reaction of superoxide free radical which is catalyzed by superoxide dismutase.

Animals↗