PubMed Health⌕ Search

Biomedical subjects

G W van Alphen

Publications and source records attributed to G W van Alphen.

At least 19 recordsLinked to original sources
PubMed1991

Elasticity of tissues involved in accommodation.

Uniaxial loading of human lens, zonules, ciliary muscle, and choroid shows a nonlinear relationship between stress and deformation of the specimen, and hysteresis on unloading. Spring constants, at 10% elongation, have been calculated for all specimens and for several combinations. Except for zonules they are significantly correlated with age. They will provide a basis for a model of accommodation. The mean force required for 10% elongation of the lens, at mean age 43, is about 22 x greater than for the zonules; and the mean elongation of the zonules is nearly 7 x that of the lens at a load of 0.01 N (approximately 1 g). Ranges of forces and pressures in the accommodated and nonaccommodated eye are estimated.

Accommodation, Ocular↗
PubMed1990

Emmetropization in the primate eye.

A theory to explain the mechanism of emmetropization of the human eye is reviewed and updated. The theory is probably also valid for the primate eye. It is proposed that the ciliary muscle-choroid layer behaves like a solid sheet of smooth muscle, so that it is able to resist part of the intraocular pressure and to regulate scleral stretch in the growing eye. It is suggested that the autonomic nervous system and stress play a role in the development of ametropia and that interference with the cortical-subcortical control of the ciliary muscle may prevent emmetropization.

Animals↗
PubMed1986

Choroidal stress and emmetropization.

Human eyes of all ages were partly denuded by removing sclera behind, in front of, or about the equator. Inflation of the eyes, up to 14 mm of Hg, was followed by axial elongation rather than the radial expansion expected. Markers proved that the elongation was the result of ciliary muscle stretch; the strain of the choroid behind the equator was so slight that tracings of the posterior segment before and after loading could be superimposed. The axial expansion of the choroid supports a crucial point in a theory of emmetropization and demonstrates the potential significance of ciliary muscle tone on choroidal tension and scleral stretch.

Adolescent↗
PubMed1985

Postjunctional adrenergic receptors in the rabbit eye: effects on uveal flow and intraocular pressure in isolated arterially perfused eyes.

In uveal vessels of isolated arterially perfused rabbit eyes there is direct evidence for the presence of post-junctional alpha 1-receptors and indirect evidence for alpha 2-receptors. Since vasoconstriction by epinephrine could not be blocked by an alpha 1-antagonist, only 30% by an alpha 2-antagonist and almost fully by the combination or by phentolamine, we suggest the presence of an intermediate alpha-type receptor which is neither alpha 1 nor alpha 2 but has characteristics of either. All alpha-types produce vasoconstriction and a fall in IOP. Of the beta-types only beta 1-receptors can be demonstrated. They mediate vasodilatation and a rise in IOP. Neither beta 2- nor non-selective beta-agonists or -antagonists (e.g. timolol) affect IOP or uveal flow.

Adrenergic alpha-Agonists↗
PubMed1985

Detergents modify uveal flow and intraocular pressure.

Detergents were administered intra-arterially to isolated arterially perfused eyes of rabbits and cats. Tween 80, Triton X-100, digitonin and sodium dodecyl sulphate (SDS) constricted uveal vessels and raised intraocular pressure (IOP) except for SDS which lowered IOP. Digitonin, a type B detergent was more active than three other detergents of type A. None of the four detergents did affect pupil size. After preconstriction with epinephrine low concentrations of nonionic detergents dilated uveal vessels but the fall in IOP by epinephrine was not affected; higher doses raised IOP. After preconstriction by eserine + Ach there were no effects of detergents on uveal flow and IOP. Mepacrine decreased the ocular effects of detergents suggesting that at least part of the effects from detergents is due to liberation of phospholipids.

Acetylcholine↗
PubMed1985

Pretreatment with detergents modulates the effects of epinephrine on uveal flow and intraocular pressure.

Prior administration of detergents modulates the effects of epinephrine (epi) in isolated, arterially perfused rabbit eyes. Pretreatment with Tween 80, Triton X-100, digitonin and sodium dodecyl sulphate (SDS) caused a dose-dependent reduction of epi induced vasoconstriction of uveal vessels. There also was a dose-dependent reduction of the epi induced fall in intraocular pressure (IOP) after pretreatment with Tween 80 and Triton X-100; digitonin and SDS enhanced the effects of epi on IOP but these effects were not dose-dependent. Significant effects of all four detergents on the efficacy of epi were irreversible. Digitonin probably increased the affinity of epi for the adrenergic receptor as shown by the decrease of the ED50-value; the three other detergents did not significantly affect the affinity. The sequence of administration of epi and detergents is of minor importance for the effects of Tween 80 and Triton X-100 but differs significantly for the effects of digitonin and SDS.

Animals↗
PubMed1985

Extraocular rectus muscles of the rabbit contain alpha 2- and beta 2-adrenergic receptors.

Selective and non-selective adrenergic drugs were given to isolated extraocular rectus muscles (EOM) of rabbits to differentiate its postjunctional adrenergic receptors. Without precontraction none of the adrenergic agents had significant effects, but after cholinergic precontraction of the muscles a further contraction could be obtained with the non-selective agonists epinephrine, norepinephrine and isoproterenol, with the alpha 2-agonist B-HT 920, and with the beta 2-agonist terbutaline. No effect was seen from alpha 1- and beta 1-agonists. The presence of alpha 2- and beta 2-receptors was confirmed in experiments with selective and non-selective adrenergic antagonists. The lack of alpha 1-receptors in EOM and the absence of a hypertensive peak after topical alpha 2- and beta 2-agonists in vivo does not support the assumption that the initial rise in intraocular pressure (IOP) after topical epinephrine is produced by contraction of EOM.

Acetylcholine↗
PubMed1984

Acetylcholine can exert two opposite effects on uveal flow in isolated arterially perfused eyes of cats and rabbits.

Acetylcholine (Ach) has an effect on IOP and uveal flow. It elevates IOP in cats but not in rabbits in eserinized preparations. A fall in IOP induced by epinephrine (epi) or norepinephrine (nor-epi) is partly reversed by the addition of Ach. Ach has a dual effect on uveal flow in both cats and rabbits. It causes vasoconstriction in high concentrations or in the presence of eserine (Es). The constriction is presumably maximal in the choroidal (efferent) part of the ciliary processes. Ach may also cause vasodilatation after preconstriction of uveal with adrenergic agents. The dilatation is probably located in the afferent vessels of the ciliary processes. The dose of Ach required for dilating preconstricted uveal vessels is at least 3 magnitudes lower than the dose for constricting the uveal vasculature. We propose that uveal vessels contain two kinds of muscarinic receptors, one inhibitory and another excitatory.

Acetylcholine↗
PubMed1982

Does prostacyclin mediate alpha-adrenergic induced hypotension?

We have extended our previous observations on the effect of tranylcypromine (TCP) on intraocular pressure (IOP), following topical administration of catecholamines is normal and chemically denervated rabbit eyes. In normal eyes, TCP inhibits the hypotensive phase after topical norepinephrine (nE); less after epinephrine (E); and not at all after isoproterenol. In denervated eyes, the inhibitory effect of TCP on the hypotensive phase of nE and E is enhanced. Phenoxybenzamine (PBA), but not timolol maleate or indomethacin, blocks the effect of TCP on alpha-adrenergic induced hypotension. Prostacyclin-like activity was estimated by bioassay using ADP induced rat platelet aggregation. This activity is significantly reduced in the primary aqueous and in the iris after TCP but it is significantly increased in pooled data of aqueous samples after topical nE. We conclude that the inhibitory effect of TCP on the hypotensive phase after topical E and nE is the result of inhibition of prostacyclin synthesis and not of MAO inhibition nor blockade of alpha-receptors. It is possible that the normal production of prostacyclin by the iris and ciliary body maintains (lower) basal levels of IOP.

Animals↗
PubMed1982

Unsaturated fatty acids alter aqueous humor dynamics and uveal flow.

We report the effects of four unsaturated fatty acids (UFAs) - arachidonic (AA), linoleic, alpha-linolenic and oleic acid - and one saturated fatty acid (stearic acid) on aqueous humor (AH) dynamics of the isolated arterially perfused cat eye. UFAs, but not stearic acid, increase inflow of AH and elevate IOP; they do not affect the size of the pupil except for AA which produces maximal constriction. Indomethacin blocks the AA induced increase in inflow and the constriction of the pupil but it does not prevent the rise in IOP; indomethacin does not block increased flow or IOP caused by linoleic acid. We conclude that the fatty acid moiety of UFAs affects the blood aqueous barrier and possibly also the outflow channels. AA has a dual effect since in addition to a general fatty acid effect, an AA induced cyclo-oxygenase product affects AH inflow and constricts the pupil. All UFAs dilate the iridial part and constrict the choroidal part of the ciliary processes; this may contribute to increased inflow of AH and elevation of IOP.

Animals↗
PubMed1981

Behaviour of IOP and pupil size after topical tranylcypromine in the rabbit eye.

Repeated topical administration of tranylcypromine (TCP) to adult rabbit eyes causes a transient rise in intraocular pressure (IOP) for one half hour and a dilatation of the pupil for more than two hours. These effects are blocked by phenoxybenzamin but not by timolol. Indomethacin blocks the rise in pressure but not the pupillary dilatation. Chemical denervation blocks both effects. The rise in IOP is not followed by a hypotensive phase. It is suggested that TCP has a dual effect on the eye. Firstly, TCP as a releaser of endogenous nor-epinephrine (nE) and as a monoamine oxydase inhibitor will induce accumulation of nE at the receptor-side which in turn probably stimulates the synthesis of PGs to raise IOP. Secondly, TCP as a prostacyclin synthase inhibitor may be responsible for the absence of a hypotensive response. This is strengthened by the finding that TCP inhibits the hypotensive response to nE but potentiates the dilatation of the pupil.

Animals↗
PubMed1980

The effects of prostaglandins on aqueous humor dynamics.

PGE2, applied topically to the cornea of enucleated, arterially perfused cat eyes, produced an increase in the rate of aqueous humor (AH) production but only minimal changes in eye pressure, as observed in vivo. In contrast, PGE1, E2 and F2 alpha, administered intrarterially, induced no change in AH productin or arterial perfusate flow rate. In eyes which the AH inflow rate had been accelerated by prior administration of acetylcholine plus eserine, PGE1, E2 and F2 alpha caused a lowering of the inflow rate as well as vascular dilatation.

Acetylcholine↗
PubMed1978

The high yield of prostacyclin biosynthesis by the iris and its effects on the intraocular muscles.

Iris, and to a lesser extent ciliary body, from cat and rabbit produce considerable amounts of prostacyclin (PGI2) after incubation of the tissue with 1-14C arachidonic acid. These tissues also generate PGI2-like material after gentle squeezing. It is likely that major metabolites found previously in iris and aqueous humor actually were 6-keto-PGF1alpha. It is concluded that PGH2 and PGI2 are synthetized at the same location. PGI2 induces a contraction of the sphincter and dilator and a relaxation of the ciliary muscle if the tissues had been previously exposed to indomethacin. Thromboxane A2 (TxA2) has either no effect or may cause a slight relaxation of the sphincter.

Animals↗
PubMed1978

Effect of prostaglandins on the blood-aqueous barrier of the perfused cat eye.

With a technique of direct visualization of the arterially perfused cat eye, the pressure head may be chosen so that fluorescein added to the perfusate just barely stains the ciliary processes. After addition of PGE1, PGE2, PGF2alpha arachidonic acid, or indomethacin, with or without PG's, no more dye emerged from the processes. The addition of acetylcholine in the eserinized eye floods the processes with dye, apparently affecting the pore size of the blood-aqueous barrier; PG's may slightly inhibit, rather than facilitate, the emergence of fluorescein from the processes. It is speculated that in the cat PG's elevate pressure and protein content by backflow from the circle of Hovius, which is the equivalent of Schlemm's canal.

Acetylcholine↗