Biomedical subjects

J W Huff

Publications and source records attributed to J W Huff.

At least 19 recordsLinked to original sources

PubMed1991

New cryoprotectant for cryorefractive surgery.

Cryorefractive surgeries, keratomileusis, keratophakia, and epikeratophakia cause destruction of keratocytes, which may result in postoperative corneal haze. We examined the effects of two cryoprotectants on keratocyte survival following freeze injury. We compared the ability of CPTES and the standard cryoprotectant KM-26 to prevent keratocyte death by altering the length of time corneal tissue was exposed to the cryoprotectant. When corneal stroma was immersed in CPTES for five minutes prior to freezing, 66.5% of the keratocytes survived; when tissue was immersed in KM-26 for the same length of time, 27.5% survived (P less than .01). Immersion for one to 30 minutes in CPTES prior to freezing produced keratocyte viabilities that were 40% to 80% of those of fresh, unfrozen tissue; immersion in KM-26 produced keratocyte viabilities of 20% to 60%. We compared the ability of these cryoprotectants to reduce corneal haze following freeze injury using our rabbit model of lamellar keratoplasty. The postoperative data were comparable to those in the cell culture experiments. Based on our findings in rabbit corneas, a cryoprotective medium such as CPTES may promote cell survival and thereby speed recovery from cryorefractive procedures in humans.

Animals↗

PubMed1991

Effects of temperature and conditioning on contact lens wetting angles.

Because wettability is not always examined under standard conditions, we investigated the temperature dependence of saline wettability on unconditioned and conditioned polymethylmethacrylate (PMMA), cellulose acetate butyrate (CAB), and three silicone acrylate lens materials. Sessile drop contact angles were measured in a humidity chamber at 23 degrees C and 34 degrees C using laser-assisted contact angle goniometry. In separate experiments, saline-stored and preconditioned lenses were examined either with or without rinsing. Sessile drop contact angles at 34 degrees C were within 2 degrees to 5 degrees of the room temperature values for both conditioned and unconditioned lenses, demonstrating a negligible temperature dependence. At both temperatures, the conditioned PMMA, CAB, silafocon A, and pasifocon C lenses wet slightly better, by 1 degree to 12 degrees, than unconditioned lenses. However, this increase was only significant with PMMA and silafocon A (P less than 0.05) and reversed when the preconditioned lenses were rinsed repeatedly in saline and reexamined. The results suggest that for these materials: 1) in vitro saline contact angles do not approach those seen on the eye, and this discrepancy can not be explained by temperature or conditioning; and 2) conditioning does not increase material wettability but merely forms a temporary hydrophilic interface that is more wettable than the lens material.

Acrylic Resins↗

PubMed1991

Studies on initiation of silicone elastomer lens adhesion in vitro: binding before the indentation ring.

We studied silicone elastomer lens binding in vitro to determine what factors may influence its development on the cornea or corneosclera. Lens binding to corneas was not influenced by corneal toricity (0-20 D), corneal fitting relationship (2 D steep to 4 D flat), mucin (2 or 5%) in the tear-bath, or transcorneal pressure (11-22 mm/Hg). In isolated corneas or in whole eyes, transient intraocular pressure changes did not influence keratometry readings, ruling these out as potential mechanisms for corneal binding during sleep. Corneoscleral preparations were also examined to simulate a decentered lens. Corneoscleral binding occurred with a significantly (P less than 0.001) greater frequency than corneal binding and was not influenced by corneal toricity, corneal fitting relationship (up to .5 mm steeper than K), or mucin concentration. Unlike the final stages of clinical lens adhesion, the binding we observed permitted lateral lens movement and occurred without leaving an indentation ring. These findings may suggest that the system models the initiation of corneoscleral binding, involving decentration and suction onto the corneoscleral junction. Corneal binding, however, cannot be explained by a chemical attraction between the silicone elastomer lens surface and cornea, with or without mucin interaction, and must be accounted for by other factors found in vivo.

Adhesiveness↗

PubMed1991

Contact lens-induced edema in vitro. Pharmacology and metabolic considerations.

The effects of physiologic and pharmacologic manipulations on contact lens-induced edema were studied. In isolated superfused rabbit corneas bathed in Ringer's solution and covered with large-diameter polymethylmethacrylate (PMMA) lenses, corneal swelling rates of 17-26 microns/hr (versus -5-5 microns/hr in paired controls) were observed. Neither the calcium antagonist diltiazem (10(-4) M), the glucocorticoid dexamethasone (10(-7) M), the glucose substitute fructose (20 mM), nor 0.5 mM adenosine and 0.3 mM reduced glutathione mitigated the edema. Lens-induced edema was 25 microns/hr in corneas bathed at pH 8.2 and decreased to 9 microns/hr at pH 7.0. In corneas without lenses, however, decreasing the pH from 7.4-7.0 caused significant swelling (P less than 0.05). The pyruvate dehydrogenase stimulant sodium dichloroacetate (3.2 mM) on the tears side ameliorated the edema, and its congener, 3.2 mM 2-chloropropionate, was less effective. These latter agents are known to relieve lactic acidosis systemically and had no significant effect on corneas without lenses. In tissues bathed with 20 mM lactate Ringer's, normal thickness was maintained in both control and PMMA-treated corneas throughout the 3-hr period. These findings suggest that the contact lens-induced edema does not involve the acute cytotoxic mechanisms seen in severe tissue ischemia or hypoxia. The edema appears to result in part from acidosis but mainly from stromal lactate accumulation.

Animals↗

PubMed1990

Contact lens-induced edema in vitro. Ion transport and metabolic considerations.

The relationship of contact lens-induced edema to epithelial and endothelial function was determined in isolated superfused rabbit corneas. Placement of a polymethyl methacrylate (PMMA) contact lens on the cornea caused swelling rates of 15-28 microns/hr compared to 0-6 microns/hr in paired control corneas. The edema increased with temperature (P less than 0.01). PMMA-induced swelling was significant in: 1) bicarbonate-free Ringer's solution; 2) chloride-free Ringer's; 3) 0.3 mM furosemide-treated corneas; and 4) deepithelialized corneas. The swelling did not occur in corneas with silicone oil replacing the endothelium to block fluid uptake. The effluent aqueous bathing fluid from edematous corneas did not induce edema in normoxic corneas. These studies demonstrate that contact lens-induced edema depends on metabolism, involves a significant stromal contribution, and requires fluid absorption across the endothelial layer, but is not a direct result of epithelial and endothelial ion transport inhibition.

Animals↗

PubMed1979

A new platelet aggregation inhibitor which possesses hypolipemic and uricosuric properties, 2-[3-(2-thiazolylthio)phenyl]propionic acid (TPA).

In vitro, 2-[3-(2-thiazolylthio)phenyl]propionic acid (TPA) at plasma concentrations ranging from 0.02 to 1.0 microgram/ml prevents aggregation of human platelets induced by various aggregating agents. Oral administration of TPA to guinea pigs inhibits platelet aggregation; the estimated dose to reduce aggregation by 50% is 0.3 mg/kg. TPA protects rabbits against arachidonate-induced thromboembolic death (50% protection at 0.79 mg/kg i.p.). TPA is a potent hypotriglyceridemic agent in rats when present in the diet in concentrations as low as 0.003%. In chimpanzees, TPA is uricosuric at oral doses of 0.625 and 2.5 mg/kg. This rare combination of pharmacological properties suggests that TPA is a potentially useful antithrombotic agent.

Adenosine Diphosphate↗

PubMed1977