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Biomedical subjects

K Green

Publications and source records attributed to K Green.

At least 145 records · Page 8Linked to original sources
PubMed1990

Ocular blood flow and vascular permeability in endotoxin-induced inflammation.

Blood flow was measured in several tissues of the rabbit eye following intravitreal injection of a dose of endotoxin that induces an inflammatory response. In separate experiments, the vascular permeability of the inflamed eye was estimated by iris fluorescein angiography and by measuring protein influx into the aqueous humor. The effect of topical corticosteroid treatment upon blood flow and vascular permeability was also measured. Following intravitreal endotoxin injection, minor changes in blood flow occurred in retina and optic nerve head. Marked changes were observed in blood flow in iris, ciliary processes, and choroid. Steroid treatment had no effect upon the increased blood flow 24 h after the endotoxin injection, although from a clinical standpoint the steroid-treated eyes appeared less inflamed. Fluorescein angiography demonstrated a massive increase in iris vessel permeability 6 and 24 h following endotoxin injection. Topical steroid treatment reduced fluorescein entry into the anterior chamber at both time periods. On the other hand, the increase in protein influx into the aqueous humor in the endotoxin-inflamed eye was not inhibited by steroid pretreatment. It is suggested that corticosteroids have a selective effect upon the permeability of different components of the blood-aqueous barrier, namely the ciliary processes and the iris vasculature.

Animals↗
PubMed1990

Effect of calcium channel blockers on intraocular pressure.

We determined the effects of either topical or systemic calcium channel antagonists on rabbit intraocular pressure (IOP). Topical nifedipine, verapamil or diltiazem had no significant effect on IOP. Intravenous verapamil and nifedipine caused statistically significant reductions in IOP between 2 and 6 h after administration; the nifedipine response followed an increase in IOP at 30 min. Diltiazem, given 3 times daily for 3 days, caused no pressure change. In the rabbit, therefore, calcium channel antagonists have no effect when given topically, but do reduce IOP when given systemically.

Animals↗
PubMed1990

Direct stimulation by succinate of Na+:K+ pump in rabbit ciliary epithelium.

The effects of succinate on the intracellular potential difference, PDI, were measured in isolated rabbit ciliary processes. Concentration-dependent increases in the hyperpolarization of PDI occurred between 1 and 15 mM succinate in NaCl Ringers. With 5 mM succinate, there was a 6 mV hyperpolarization. Even though the hyperpolarization of PDI was comparable with 10 and 15 mM succinate, it was more sustained at the latter two concentrations. Succinate also elicited comparable hyperpolarizations of PDI in either Cl(-)-free or HCO3(-)-free Ringers. Similarly, following incubation with either 0.1 mM DIDS or 3 mM BaCl2 the effect of succinate on PDI was unchanged. Five mM succinate had no effect if it was added after 5 mM malonate. Malonate (5 mM) rapidly reversed a 5 mM succinate-induced hyperpolarization of PDI which also suggests a metabolically mediated effect on PDI. An isosmotic substitution of Na+ with NMDG Ringers depolarized PDI, whereas PDI depolarized biphasically during exposure to 0.1 mM ouabain. The addition of 5 mM succinate had no effect on either the time course or the magnitude of the depolarization of PDI during blocking of the Na+:K+ pump with either Na(+)-free Ringers or ouabain. Taken together, these results show that succinate selectively stimulates the Na+:K+ pump, but has no effect on any Cl-, HCO3- or a Ba2(+)-sensitive K+ conductance.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1990

Effects of adrenergic drugs on intracellular electrical potential difference of rabbit ciliary epithelial cells.

The effects of adrenergic drugs on intracellular electrical potential difference (PDI) of rabbit ciliary epithelial cells were investigated. Epinephrine as well as norepinephrine hyperpolarized the PDI at lower concentrations (10(-6) M) and depolarized the PDI at higher concentrations (greater than 10(-5) M). Isoproterenol produced a depolarization of PDI and phenylephrine caused a hyperpolarization only. After pretreatment with propranolol, the change of PDI by isoproterenol was minimal. Selective agonists and antagonists were used to further characterize adrenergic effects on the PDI. Both beta 1 and beta 2 agonists caused a depolarization of PDI while both beta 1 and beta 2 antagonists produced a hyperpolarization. Alpha 1 antagonist depolarized the PDI and alpha 2 antagonist hyperpolarized the PDI. Such electrophysiological effects of the adrenergic drugs confirm the presence of alpha and beta adrenoceptors in the rabbit ciliary epithelial cells.

Adrenergic alpha-Agonists↗
PubMed1990

Bicarbonate and DIDS effects on intracellular potential difference in rabbit ciliary epithelium.

A change of [HCO3-] in the solution bathing isolated rabbit ciliary epithelium from 30 mM to 0, or vice versa, resulted in a change of intracellular electrical potential difference (PDI) of 7 mV. Intermediate [HCO3-] (5, 10 and 15 mM) solutions were also tested. No perceivable change of PDI occurred when [HCO3-] changed from 30 to 15 mM. PDI depolarized gradually when [HCO3-] decreased from 30 or 15 mM to 0 mM, but PDI hyperpolarized at a faster rate when [HCO3-] increased from 0 to 15 or 30 mM. The amount of change of PDI from 15 to 5 mM, or vice versa, and from 10 to 0 mM or vice versa, was 4 mV. The stilbene, DIDS (10(-4) M), hyperpolarized the PDI in HCO3(-)-rich solutions. The response of DIDS was reduced in HCO3(-)-free medium and inhibited in Cl(-)-free solution. The results suggest the existence of an electrogenic bicarbonate transport or Na+/HCO3- cotransport system.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1990

Effects of silicone oils on corneal endothelial permeability.

Silicone oils, varying by viscosity and manufacturer, were infused into rabbit anterior chambers. Polydimethyl-siloxane oil, 5000 cps, increased corneal endothelial permeability to inulin (mw 5000) and dextran (mw 60000) when measured in vitro at 1, 4 and 7 days after ocular infusion. The effects of five other oils were measured at 7 days after infusion. Four of the oils increased endothelial permeability and induced similar morphological changes. Dow Corning Medical Fluid 360 had no effect on either permeability or morphology of the endothelium. These results show that contact of most silicone oils with corneal endothelium rapidly induces physiological and morphological changes. If these oils, when used as a retinal tamponade, gain access to the cornea they should be removed quickly to avoid the rapid initiation of physiologic changes.

Animals↗
PubMed1990

Role of glutathione in the regulation of anterior chamber hydrogen peroxide.

Catalase inhibition leads to an increase in the t 1/2 for hydrogen peroxide loss from the anterior chamber and increased tissue damage. BCNU (1,3-bis-(2-chloroethyl)-l-nitrosourea) and BSO (buthionine sulfoxamine) were used to suppress glutathione reductase and glutathione synthesis, respectively. Intravitreal BSO (1 to 4 mg) reduced total glutathione levels of iris by 80%, and aqueous glutathione levels by 70%. BSO caused the t 1/2 for hydrogen peroxide disappearance from the anterior chamber to increase after 10 microliters of 10 mM peroxide was injected intracamerally but not after 25 or 50 mM peroxide injections. Catalase inhibition, however, had more influence at 50 mM than with 10 or 25 mM injections. The glutathione redox system is operative at low aqueous hydrogen peroxide concentrations and catalase is of greater importance at higher peroxide concentrations.

Amitrole↗
PubMed1990

Techniques of intraocular pressure determination.

A variety of indentation or applanation tonometers are available for the measurement of intraocular pressure in conscious or anesthetized animals. The Schiøtz tonometer is a simple indentation tonometer, but unless used properly can give misleading values. Applanation tonometers include the air tonometer, pneumatonograph, and the Goldmann type (either slit-lamp or hand-held models). These flatten a small, fixed area of cornea and measure the resultant pressure. In anesthetized animals anterior chamber cannulation may be performed, although breakdown of the blood-aqueous barrier can ensue together with an alteration of intraocular pressure. Of importance is that all tonometers be calibrated for each species since scleral rigidity, ocular curvature, pressure/volume relationships, etc. all vary between species.

Humans↗
PubMed1990

Toxicity of intracameral thymoxamine.

The anterior chamber of adult pigmented rabbits was perfused with 1 ml of either 0.02% or 0.2% thymoxamine hydrochloride in Balanced Salt Solution. Contralateral eyes were either perfused with BSS alone or remained untouched. Measurements were made of corneal thickness and intraocular pressure prior to perfusion and at days 1, 2, 3 and 7 after perfusion. Observations were made of toxic reactions of ocular tissues using slit-lamp biomicroscopy. No effects were noted with 0.02% thymoxamine but 0.2% caused corneal swelling and a reduction in intraocular pressure at day 1. Neither concentration caused any observable toxic responses. Morphologic studies confirm the absence of effects by 0.02% thymoxamine, and that 0.2% causes disturbance of both corneal endothelium and iris-ciliary processes. This data, together with an earlier report on in vitro studies of thymoxamine, allows the conclusion that 0.02% thymoxamine is a safe concentration for use in the anterior chamber and 0.2% yields adverse reactions.

Animals↗
PubMed1990

Morphologic and physiologic effects of thymoxamine on corneal endothelium and ciliary processes.

Either 0.2 or 0.02% thymoxamine hydrochloride was perfused across the endothelium of isolated rabbit corneas in a specular microscope. Treated corneas did not swell, compared to controls, when perfused with 0.02% thymoxamine, but swelled at 34 microns/hr after 0.2% thymoxamine compared to 10 microns/hr of controls. Morphologically, 0.2% thymoxamine caused many intracellular vacuoles, with far fewer changes after 0.02%. Replacement of the aqueous humor with 0.02% thymoxamine caused no effect on either the corneal endothelium or ciliary process, whereas 0.2% caused small, but significant, changes in both tissues.

Animals↗
PubMed1990

Role of eicosanoids in the ocular response to intracameral hydrogen peroxide.

The intracameral injection of hydrogen peroxide induces a sequence of responses in the tissues bounding the anterior chamber. These changes include intraocular pressure, corneal thickness, iris hyperemia, increased leakiness of the iris vasculature, and edema of the ciliary processes as judged from microscopic examination. Some of these responses appear to include inflammatory effects that may be the result of the local release of eicosanoids. Several antagonists of the arachidonic acid cascade, indomethacin, aspirin, dexamethasone, and nordihydroguaiaretic acid (NDGA) were used to examine their influence on the sequelae of hydrogen peroxide injection. Indomethacin, and high dose (7.5 mg/kg) NDGA were most effective in reducing the number of parameters that were altered after intracameral hydrogen peroxide. Microscopic observations supported the physiological changes and the responses to antagonists. The data indicate that a portion of the ocular tissue responses to intracameral hydrogen peroxide in the rabbit eye may be the result of eicosanoid production in these tissues.

Animals↗
PubMed1990

Effect of PO2 and metabolic inhibitors on ionic fluxes across the isolated rabbit corneal endothelium.

Bicarbonate and sodium fluxes were measured across the isolated rabbit corneal endothelium under the influence of several inhibitors. Depression of PO2 in the bathing medium decreased net sodium movement but increased bicarbonate movement. Furosemide did not alter bicarbonate fluxes at either 10(-4) or 10(-5) M, but increased passive sodium flux leading to a decrease in net flux. Thiocyanate, at 5 x 10(-3) or 5 x 10(-2) M, decreased active bicarbonate flux and hence net flux, but had no effect on sodium fluxes. Dinitrophenol increased only the passive bicarbonate flux while decreasing both active and passive sodium fluxes, albeit unequally, leading to a decreased net flux. Ethacrynic acid affected only passive bicarbonate flux, while decreasing net sodium flux. The stilbene derivatives, SITS and DIDS caused opposite effects on both sodium and bicarbonate fluxes. SITS decreased net bicarbonate flux by decreasing active and increasing passive flux, yet increased net sodium flux. DIDS, however, increased net bicarbonate flux but decreased net sodium flux. The results may be explained by current models for endothelial ion transport that include a Na+/H+ antiport and a HCO3-/Na+ symport system in parallel with an independent pathway for HCO3- exit from the endothelial cells. When compared with prior corneal swelling data using these same inhibitors, the maintenance of corneal thickness appears to be dependent on the variation of ion fluxes from normal values, and the dissociation of the two active ion fluxes. In addition, there appears to be a significant ability of ion transport systems to compensate for disturbances to other ion exchange or transport mechanisms.

Animals↗
PubMed1989

VP4 protein of porcine rotavirus strain OSU expressed by a baculovirus recombinant induces neutralizing antibodies.

The complete VP4 gene of porcine rotavirus strain OSU has been inserted into a baculovirus expression vector under the control of the polyhedrin promoter. The VP4 outer capsid protein, which is a major neutralization antigen in rotavirus, was expressed in high yield in Spodoptera frugiperda cells. Reactivity with polyclonal and monoclonal antibodies suggested that neutralizing epitopes were functionally unaltered on the expressed VP4. The VP4 produced in this system also induced antibodies in guinea pigs which inhibited hemagglutination of OSU and neutralized its infectivity to high titer. The available evidence suggests that the VP4 expressed in insect cells maintained its antigenic configuration and may prove useful in elucidation of (1) the extent of VP4 polymorphism among human and animal rotaviruses and (2) the distribution of VP4 among these viruses.

Animals↗
PubMed1989

Effect of acetyl salicylic acid on increased production of thromboxane after aortic graft surgery.

Contact between blood and foreign surfaces, e.g. vascular grafts, causes activation and release of platelets. One consequence of platelet activation is production of thromboxane A2 (TxA2). The physiological effects of TxA2, i.e. platelet aggregation and vaso-constriction are counteracted by another prostanoid, prostacyclin (PGI2). Acetylsalicylic acid (ASA) causes a longlasting inhibition of platelet TxA2 production and a more shortlasting inhibition of PGI2 production. The present study examines TxA2 and PGI2 synthesis in patients receiving synthetic arterial grafts, some of which were treated with ASA. The prostanoid synthesis was evaluated by measurement of their main urinary metabolites with gas chromatography-mass spectrometry. Platelet release was evaluated by measurements of beta-thromboglobulin (beta-TG) and the plasma coagulation by measurements of fibrinopeptide A (FPA). These compounds were also measured in urine in order to avoid artifacts caused by activation of platelets and plasma coagulation during blood sampling. Following replacement of the abdominal aorta with a synthetic vascular graft there was a marked increase in the synthesis of TxA2 and PGI2. Increased levels of beta-TG and FPA were also demonstrated. Administration of ASA on the first and second postoperative days significantly reduced the synthesis of TxA2 but caused no significant effects on the other parameters measured. It is concluded that ASA may be beneficial in the postoperative period since it counteracts TxA2 with vasoconstricting and platelet aggregating properties but leaves PGI2 with vasodilating and antiaggregating properties relatively uneffected.

Aged↗
PubMed1989

Topical dexamethasone lowers rabbit ocular tension, as does topical mifepristone (RU 486), a peripheral blocker of dexamethasone and progesterone.

The variability of the response of the rabbit eye to topical 1% dexamethasone has been shown in two groups of 20 young albino rabbits each (total 40) tested in succession. The pressure anomalously fell significantly (but by only 1 mm Hg) in both groups in the first 4 weeks of administration, but not in subsequent weeks. Mifepristone (RU 486), a peripheral antagonist of dexamethasone and progesterone, reduced the pressure significantly, again by only 1 mm Hg, in the first group of 20 rabbits, not the second. Accordingly, no conclusion was possible on the originating question: does pre-treatment with mifepristone prevent the dexamethasone-induced rise in rabbit intra-ocular pressure?

Administration, Topical↗