Effect of Aqueous Dynamics on Gas Behavior Following Retinal Reattachment Surgery.

BACKGROUND AND OBJECTIVE: To determine how the gas concentration in air required to achieve full postoperative vitreous cavity fill varies in different aqueous outflow states. MATERIALS AND METHODS: A mathematical model was used to estimate gas dynamics. The change in gas bubble volume over time was calculated in an eye with normal aqueous outflow, ocular hypertension (OHT), and OHT with apraclonidine treatment. RESULTS: The concentration required was higher for all gases to achieve a full postoperative fill in OHT eyes versus normal eyes. Optimal gas concentrations were 22.6% for SF6, 13.9% for C2F6, and 11.6% for C3F8. Despite this, in OHT, the fill achieved was 95%, 95%, and 94% for SF6, C2F6, and C3F8, respectively. With apraclonidine, percentage fill improved for all gases. CONCLUSIONS: This is the first study to show aqueous outflow affects bubble size and indicates eyes with reduced outflow are at risk of underfill. This can ultimately affect surgical success. [Ophthalmic Surg Lasers Imaging Retina. 2020;51:522-528.].

THEORETICAL GAS CONCENTRATIONS ACHIEVING 100% FILL OF THE VITREOUS CAVITY IN THE POSTOPERATIVE PERIOD: A Gas Eye Model Study.

PURPOSE: To determine the concentrations of different gas tamponades in air to achieve 100% fill of the vitreous cavity postoperatively and to examine the influence of eye volume on these concentrations. METHODS: A mathematical model of the mass transfer dynamics of tamponade and blood gases (O2, N2, and CO2) when injected into the eye was used. Mass transfer surface areas were calculated from published anatomical data. The model has been calibrated from published volumetric decay and composition results for three gases sulphahexafluoride (SF6), hexafluoroethane (C2F6), or perfluoropropane (C3F8). The concentrations of these gases (in air) required to achieve 100% fill of the vitreous cavity postoperatively without an intraocular pressure rise were determined. The concentrations were calculated for three volumes of the vitreous cavity to test whether ocular size influenced the results. RESULTS: A table of gas concentrations was produced. In a simulation of pars plana vitrectomy operations in which an 80% to 85% fill of the vitreous cavity with gas was achieved at surgery, the concentrations of the 3 gases in air to achieve 100% fill postoperatively were 10% to 13% for C3F8, 12% to 15% for C2F6, and 19% to 25% for SF6. These were similar to the so-called "nonexpansive" concentrations used in the clinical setting. The calculations were repeated for three different sizes of eye. Aiming for an 80% fill at surgery and 100% postoperatively, an eye with a 4-mL vitreous cavity required 24% SF6, 15% C2F6, or 13% C3F8; 7.2 mL required 25% SF6, 15% C2F6, or 13% C3F8; and 10 mL required 25% SF6, 16% C2F6, or 13% C3F8. When using 100% gas (e.g., used in pneumatic retinopexy), to achieve 100% fill postoperatively, the minimum vitreous cavity fill at surgery was 43% for SF6, 29% for C2F6, and 25% for C3F8 and was only minimally changed by variation in the size of the eye. CONCLUSION: A table has been produced, which could be used for surgical innovation in gas usage in the vitreous cavity. It provides concentrations for different percentage fills, which will achieve a moment postoperatively with a full fill of the cavity without a pressure rise. Variation in axial length and size of the eye does not seem to alter the values in the table significantly. Those using pneumatic retinopexy need to increase the volume of gas injected with increased size of the eye to match the percentage fill of the vitreous cavity recommended for a given tamponade agent.

Physiological-based pharmacokinetic modeling of endotoxin in the rat.

We have previously measured the distribution and pharmacokinetics of biosynthetically radiolabeled endotoxin of Salmonella typhimurium following intraperitoneal (IP) dosing (200 µg/kg) in Sprague-Dawley rats. In our experiments, the fatty acid residues were labeled with (3)H and the glucosamine residues were labeled with (14)C. To predict the dynamics of endotoxin exposure, we developed a physiological-based pharmacokinetic model using our measured distribution results. The model was validated with published low-dose (30 µg/kg) IP exposure results in rats. Endotoxin pharmacokinetics depended on dose and route. At high IP doses, absorption was followed by biphasic decay over 48 h in plasma. There were tissue accumulations of the fatty acid and glucosamine residues in various target organs, including the brain. We also found that the glucosamine and fatty acid components separated in vivo about 3 h after IP injection. At the lower IP dose, a smaller fraction of the dose was distributed to the tissues, with most of the dose remaining in the blood. Each component had its own dynamic behavior and target tissue distribution in the rat. The fatty acid components tended to remain in the brain stem, caudate nucleus, cerebellum, frontal cortex, hippocampus, and hypothalamus. Other organs (spleen, kidney, meninges, and choroid plexus) had similar biphasic distribution. The liver had the unique accumulation of both glucosamine and fatty acid residues.

Distribution and pharmacokinetics of double-radiolabeled endotoxin in the rat brain and peripheral organs.

The endotoxin, lipopolysaccharide (LPS), of Salmonella typhimurium was biosynthetically labeled with (3)H and (14)C incorporated into the fatty acyl chains and glucosamine residues, respectively. The radio-labeled LPS was isolated from the bacteria and then injected into Sprague-Dawley rats. The distribution of (14)C and (3)H-LPS in plasma and other organs was determined following intraperitoneal (IP) doses of (14)C and (3)H-LPS (200 µg/kg). Plasma concentrations of both fatty acyl chains and glucosamine residues were biphasic, with a relatively rapid decay followed by a slow decline for 48 h. Similar biphasic results were found in the peripheral organs (kidney and heart) and brain barrier tissues (meninges and choroid plexus). In other brain tissues (brain stem, caudate nucleus, hypothalamus, frontal cortex, cerebellum and hippocampus), the glucosamine residue was biphasic, whereas the fatty acyl chains showed accumulation. Highest concentrations of LPS were found in the plasma, spleen and the liver. In addition, in the liver, sustained elevations of (14)C-glucosamine and (3)H-fatty acyl chains were observed. This indicates LPS accumulation in the liver. By contrast, the spleen showed biphasic decay of glucosamine residues and accumulation of fatty acyl chains. In the brain barrier tissues, peak LPS concentrations were significantly reduced (about 70%) and were further reduced (about 95%) in other brain tissues. The high elevation of LPS in the spleen is considered indicative of an immune response. Our findings highlight the potential significant role of lipid A as shown with the sustained elevation of (3)H-fatty acyl chains in the brain.

4. Contemporary research in contact lens care.

As our understanding of the eye and how it works evolves, we must re-evaluate previous findings, beliefs, and methods of diagnosis and treatment. The eye has proven to be naturally adept at protecting itself from pathogenic intruders, but contact lens wear and lens cleaning products can adversely impact this innate ability. Keeping up to date on the latest information is challenging, and becomes more complex when trying to incorporate the new scientific data into clinical practice. Several factors prevent drawing a straight line from study findings to real-world results, such as patient compliance and potentially flawed diagnostic tools. In this section, we review the latest research findings and opinions related to contact lens care and further explore compliance and its effect on ocular health.

Material properties that predict preservative uptake for silicone hydrogel contact lenses.

OBJECTIVES: To assess material properties that affect preservative uptake by silicone hydrogel lenses. METHODS: We evaluated the water content (using differential scanning calorimetry), effective pore size (using probe penetration), and preservative uptake (using high-performance liquid chromatography with spectrophotometric detection) of silicone and conventional hydrogel soft contact lenses. RESULTS: Lenses grouped similarly based on freezable water content as they did based on total water content. Evaluation of the effective pore size highlighted potential differences between the surface-treated and non-surface-treated materials. The water content of the lens materials and ionic charge are associated with the degree of preservative uptake. CONCLUSIONS: The current grouping system for testing contact lens-solution interactions separates all silicone hydrogels from conventional hydrogel contact lenses. However, not all silicone hydrogel lenses interact similarly with the same contact lens solution. Based upon the results of our research, we propose that the same material characteristics used to group conventional hydrogel lenses, water content and ionic charge, can also be used to predict uptake of hydrophilic preservatives for silicone hydrogel lenses. In addition, the hydrophobicity of silicone hydrogel contact lenses, although not investigated here, is a unique contact lens material property that should be evaluated for the uptake of relatively hydrophobic preservatives and tear components.

A dynamic simulation of bisphenol A dosimetry in neuroendocrine organs.

Bisphenol A (BPA) is a known xenoestrogen with similar properties to 17beta-estradiol. BPA and estrogen are hydrophobic compounds, and this affects the pharmacokinetics of both compounds in mammals. In a previous study we measured the distribution of BPA in female F344 rats exposed to oral doses of 0.1, 10 and 100 mg/kg. The results showed distribution to target neuroendocrine organs at all doses tested. Using these results, we developed a pharmacokinetic model to predict the dynamic uptake and excretion of BPA by various routes of exposure (po, iv, sc, ip). The model was able to simulate the entire time course (48 h) following various routes of exposure in rats over the dose ranges tested. The model indicated that the ultimate tissue uptake of BPA was established by the rapid initial transfer of free BPA into tissues. After free BPA enters the systemic circulation, metabolism and excretion reactions cause a relatively short duration and rapid decline. This period is followed by a slower long-term decline characteristic of BPA's biphasic pharmacokinetics. Plasma protein and tissue binding reactions established the long-term half-life of BPA in the body. Route differences in tissue uptake were directly related to the competition between transfer and binding reactions during the absorption phase.